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Chick-fil-A same-sex marriage controversy
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"Chick-Fil-A Appreciation Day" held on August 1, 2012 in Port Charlotte, Florida.
The Chick-fil-A same-sex marriage controversy was focused on the American fast food restaurant Chick-fil-A following a series of public comments made in June 2012 by chief operating officer Dan T. Cathy opposing same-sex marriage.
This followed reports that Chick-fil-A's charitable endeavor, the S. Truett Cathy-operated WinShape Foundation, had donated millions of dollars to political organizations seen by LGBT activists as hostile to LGBT rights. Activists called for protests and boycotts, while supporters of the restaurant chain and opponents of same-sex marriage ate there in support of the restaurant. National political figures both for and against the actions spoke out and some business partners severed ties with the chain.
The outcome of the controversy was mixed, as Chick-fil-A's sales rose 12 percent, to $4.6 billion, in the period immediately following the controversy. However, Chick-fil-A released a statement in July 2012 stating, "Going forward, our intent is to leave the policy debate over same-sex marriage to the government and political arena."[1] In March 2014, tax filings for 2012 showed the group stopped funding all but one organization which had been previously criticized.[2] As of April 2018, Chick Fil-A reportedly continues to donate to anti-LGBT groups.[3][4][5][6]
Contents
1 History
1.1 Group contributions from opponents of LGBT causes
1.2 Statements by Dan Cathy
1.3 Policy changes
2 Expansion to Toronto
3 Controversy
3.1 Local government
3.2 Backlash
3.3 Corporate partners
3.4 Chick-fil-A Appreciation Day
3.5 Public polling
3.6 Others
3.7 Financial effect
4 References
History[edit]
Group contributions from opponents of LGBT causes[edit]
In January 2011, the media reported that the American fast food restaurant chain Chick-fil-A was co-sponsoring a marriage conference along with the Pennsylvania Family Institute (PFI), an organization that had filed an amicus brief against striking down Proposition 8 in California (see Perry v. Brown).[7] The PFI lobbied against a state effort to ban discrimination in Pennsylvania on the basis of sexual orientation or gender identity.[8] Responding on its official company Facebook page, Chick-fil-A said that support of the PFI retreat had come from a local franchisee, stating "We have determined that one of our independent restaurant operators in Pennsylvania was asked to provide sandwiches to two Art of Marriage video seminars."[9]
The WinShape Foundation, a charitable endeavor of Chick-fil-A founder S. Truett Cathy and his family, stated that it would not allow same-sex couples to participate in its marriage retreats.[10] Chick-fil-A gave over $8 million to the WinShape Foundation in 2010.[11] Equality Matters, an LGBT watchdog group, published reports of donations by WinShape to organizations that the watchdog group considers anti-gay, including $2 million in 2009, $1.9 million in 2010 and a total of $5 million since 2003, including grants to the Family Research Council and Georgia Family Council. WinShape contributed grants to the Fellowship of Christian Athletes, and Exodus International, an organization noted for supporting ex-gay conversion therapy.[12]
Protestors at a Memphis, Tennessee Chick-fil-A store on Same Sex Kiss Day
The Marriage and Family Foundation received $994,199 in 2009[13] and $1,188,380 in 2010. The Family Research Council, an organization listed as an anti-gay hate group by the Southern Poverty Law Center in Winter 2010,[14] received $1000.[15]
Tax filings for 2012 showed that Chick-fil-A created a new foundation, the Chick-fil-A Foundation, to provide grants to outside groups. It funded only one previously funded group, the Fellowship of Christian Athletes. Other filings for WinShape Foundation showed no funding for groups opposed to LGBT causes.[2]
Statements by Dan Cathy[edit]
On June 16, 2012, while on the syndicated radio talk show, The Ken Coleman Show, Chick-fil-A president and chief operating officer (COO) Dan Cathy stated:
I think we are inviting God's judgment on our nation when we shake our fist at Him and say, "We know better than you as to what constitutes a marriage". I pray God's mercy on our generation that has such a prideful, arrogant attitude to think that we have the audacity to define what marriage is about.[16][17][18]
The following month, on July 2, Biblical Recorder published an interview with Dan Cathy, who was asked about opposition to his company's "support of the traditional family." He replied: "Well, guilty as charged."[19][20] Cathy continued:
"We are very much supportive of the family — the biblical definition of the family unit. We are a family-owned business, a family-led business, and we are married to our first wives. We give God thanks for that. ... We want to do anything we possibly can to strengthen families. We are very much committed to that," Cathy emphasized. "We intend to stay the course," he said. "We know that it might not be popular with everyone, but thank the Lord, we live in a country where we can share our values and operate on biblical principles."[19]
The day after the Supreme Court of the United States struck down Section 3 of the Defense of Marriage Act, Cathy tweeted, "Sad day for our nation; founding fathers would be ashamed of our gen. to abandon wisdom of the ages re: cornerstone of strong societies." The tweet was subsequently deleted, but was archived by Topsy.[21][22]
In March 2014, Cathy said he regretted drawing his company into the controversy.[23] He told the Atlanta Journal-Constitution he has been working with Shane Windmeyer of Campus Pride since 2012. The article noted that WinShape and the Chick-fil-A Foundation had "dramatically" cut donations to groups opposed by same-sex marriage supporters.[24]
Policy changes[edit]
In September 2012, The Civil Rights Agenda (TCRA) announced that Chick-fil-A has "ceased donating to organizations that promote discrimination, specifically against LGBT civil rights". According to the TCRA, Chick-fil-A officials stated in an internal document that they "will treat every person equally, regardless of sexual orientation."[25]
In a letter from Chick-fil-A's Senior Director of Real Estate, the company stated: "The WinShape Foundations is now taking a much closer look at the organizations it considers helping, and in that process will remain true to its stated philosophy of not supporting organizations with political agendas."[26]
According to Chicago Alderman Proco "Joe" Moreno, Chick-fil-A has a statement of respect for all sexual orientations in an internal document called Chick-fil-A: Who We Are and has promised that its not-for-profit arm, WinShape, will not contribute money to groups that oppose gay marriage.[27]
According to Focus on the Family website, CitizenLink.com: "Contrary to reports first made by the gay-activist group The Civil Rights Agenda (TCRA) on Tuesday and later picked up by mainstream media outlets, Chick-fil-A and its charitable-giving arm, the WinShape Foundation, did not agree to stop making donations to groups that support the biblical definition of marriage in exchange for being allowed to open a franchise in Chicago."[28]
Former Arkansas Governor and FOX News commentator Mike Huckabee claimed on September 21, 2012 that he had "talked earlier today personally with Dan Cathy, CEO of Chick-fil-A about the new reports that Chick-fil-A had capitulated to demands of the supporters of same sex marriage. This is not true. The company continues to focus on the fair treatment of all of its customers and employees, but to end confusion gave me this statement." The statement provided by Chick-fil-A was posted on Huckabee's website but the company did not respond to requests for comment.[29] In March 2014, new tax filings from 2012 showed that the company had stopped funding all but one organization which had been previously criticized by LGBT activists and supporters but, that group received just $25,390.[30] The company created a new foundation, the Chick-fil-A Foundation, to fund outside groups. WinShape Foundation's 2012 tax filings showed funding only for its own programs, a Berry College scholarship fund, and Lars WinShape, a home for needy children in Brazil.[2]
In 2017, Chick-fil-A is warning all its franchisees against speaking out publicly or getting involved in anything that could blur the line between their private beliefs and their public roles as extensions of the Chick-fil-A brand, the company has said.
Last year, that message extended to politics, in part to keep the brand from being exploited by candidates. The company turned down several candidates who tried to use Chick-fil-A to bolster their campaigns, according to David Farmer, Chick-fil-A's vice president of menu strategy and development.
"There are several candidates who would like to use us as a platform," Farmer told Business Insider last year. "We are not engaging. Chick-fil-A is about food, and that's it."
The company still encourages its franchisees to get "entrenched" in their communities. Operators' involvement in their communities is a critical part of what has helped Chick-fil-A attract a passionate following.
Traditionally, that has meant getting involved in local churches. But although Chick-fil-A says its focus now — both for local and corporate involvement and philanthropy — is on youth and education causes,[31], Chick-fil-A's associated foundation continues to donate hundreds of thousands of dollars a year to causes characterized as anti-gay.[32]
Expansion to Toronto[edit]
Chick-Fil-A announced their expansion to Canada in the city of Toronto.[33] This caused a number of boycotts and backlash from Canadians due to the huge support of LGBT in Canada, telling the company that they were not welcome in Canada with homophobia and transphobia.[34] As of July 2018, Chick-Fil-A still plans to open in Toronto.[33]
Controversy[edit]
Local government[edit]
After the publication of Cathy's interviews, Democrat Thomas Menino, the Mayor of Boston, stated that he would not allow the company to open franchises in the city "unless they open up their policies."[35] Menino subsequently wrote a letter to Dan Cathy, citing Cathy's earlier statement on The Ken Coleman Show, and responded: "We are indeed full of pride for our support of same sex marriage and our work to expand freedom for all people."[36]
In Chicago, Democratic alderman Proco "Joe" Moreno announced his determination to block Chick-fil-A's bid to build a second store in the city: "They'd have to do a complete 180", Moreno said in outlining conditions under which he would retract the block. "They'd have to work with LGBT groups in terms of hiring, and there would have to be a public apology from [Cathy]."[37] Moreno received backing from Chicago's Mayor, Rahm Emanuel: "Chick-fil-A values are not Chicago values", Emanuel said in a statement. "They disrespect our fellow neighbors and residents. This would be a bad investment, since it would be empty."[37]
San Francisco soon followed suit on July 26 when mayor Democrat Edwin M. Lee tweeted, "Very disappointed #ChickFilA doesn't share San Francisco's values & strong commitment to equality for everyone." Lee followed that tweet with "Closest #ChickFilA to San Francisco is 40 miles away & I strongly recommend that they not try to come any closer."[38]
The proposed bans in Boston and Chicago drew criticism from some liberal pundits, legal experts, and the American Civil Liberties Union (ACLU). Kevin Drum of Mother Jones magazine said "[T]here's really no excuse for Emanuel's and Menino's actions... you don't hand out business licenses based on whether you agree with the political views of the executives. Not in America, anyway ... what makes this whole situation so weird is that Chick-fil-A President Dan Cathy has always opposed gay marriage. He's a devout Southern Baptist, just like his father, who founded the company. The place is closed on Sundays, for crying out loud. There's just nothing new here."[39] UCLA law professor and blogger Eugene Volokh observed, "[D]enying a private business permits because of such speech by its owner is a blatant First Amendment violation."[40]
Echoing those views were Glenn Greenwald of Salon, professor John Turley of George Washington University, Adam Schwartz, a senior attorney with the ACLU, and Michael C. Dorf, the Robert S. Stevens Professor of Law at Cornell University Law School.[41][42]
Backlash[edit]
Students at several colleges and universities launched efforts to ban or remove the company's restaurants from their campuses. On November 3, 2011, New York University's Student Senators Council voted 19 to 4 to retain the Chick-fil-A franchise on campus. This vote came before a petition with over 11,000 signatures opposing its presence on campus was sent to the student council.[43] Christine Quinn, a lesbian politician and then-Speaker of the City Council who was seeking the nomination as Democratic candidate for the mayoralty in the next election, was outspoken in her opposition to keeping the Chick-fil-A franchise or allowing others, and wrote a letter to this effect to NYU President John Sexton on official letterhead, opening with the words, "I write as the Speaker of the NYC Council", urging NYU to evict a Chick-fil-A due to Cathy's opposition to same-sex marriage.[44][45]
On February 28, 2012, Northeastern University's Student Senate passed a resolution to cancel plans for a Chick-fil-A franchise on its campus, stating "the student body does not support bringing CFA [Chick-fil-A] to campus", and "Student concerns reflected CFA's history of donating to anti-gay organizations." The vote was 31 to 5, with 8 abstaining. The restaurant chain was finalizing a contract to bring it to NU when students protested.[46] Davidson College in North Carolina announced on August 13, 2012 that, in response to a petition which received 500 signatures, the school would stop serving Chick-fil-A on campus at the monthly "After Midnight" events.[47]
Other forms of protest occurred. Gay rights activists organized a "Kiss Off" to occur on August 3,[48] an event where LGBT individuals would show affection in public,[49] but it attracted smaller-than-hoped-for crowds.[50]
On August 15, 2012, a gunman attempted to enter the Washington, D.C. headquarters of the Family Research Council, carrying 15 Chick-fil-A sandwiches, a 9 mm handgun, and a box of ammunition. He shot a security guard in the left arm, and following his arrest he told police that he wanted to use the sandwiches to "make a statement against the people who work in that building ... and with their stance against gay rights and Chick-fil-A",[51] and that he planned "to kill as many people as I could ... then smear a Chicken-fil-A [sic] sandwich on their face".[52]
Corporate partners[edit]
In response to the July 2 interview, the Jim Henson Company, which had entered its Pajanimals in a kids' meal toy licensing arrangement in 2011, said that it would cease its business relationship with Chick-fil-A, and donate payment for the brand to Gay & Lesbian Alliance Against Defamation (GLAAD).[53][54][55] Citing safety concerns, Chick-fil-A stopped distributing the toys.[56] A spokeswoman stated the decision had been made on July 19 and was unrelated to the controversy.[57]
In August 2012, petitions with over 80,000 signatures were delivered to publisher HarperCollins[58] demanding the publisher cut plans to include Berenstain Bears titles as part of a kids' meal promotion. Upon being presented with petitions demanding that Berenstain Bears be pulled from a Chick-fil-A promotion, HarperCollins issued a statement saying "We have a long history of diversity and inclusiveness and work tirelessly to protect the freedom of expression. It is not our practice to cancel a contract with an author, or any other party, for exercising their first amendment rights."[59]
Chick-fil-A Appreciation Day[edit]
In response to the controversy, former Arkansas Governor Mike Huckabee initiated a Chick-fil-A Appreciation Day movement to counter a boycott of Chick-fil-A launched by same-sex marriage activists.[60][61][62] More than 600,000 people RSVPed on Facebook for Huckabee's appreciation event.[61]
On August 1, 2012, Chick-fil-A restaurants experienced a large show of public support across the nation with the company reporting record-breaking sales.[60][61][62] A consulting firm projected that the average Chick-fil-A restaurant increased sales by 29.9 percent and had 367 more customers than a typical Wednesday.[63]
Public polling[edit]
In August 2012, Rasmussen Reports published the results of a telephone survey indicating that 61 percent of likely voters held a favorable view of Chick-fil-A, while 13 percent indicated they would participate in a boycott.[64]
Others[edit]
Other notable public figures came to Chick-fil-A's defense, including former Alaska Governor Sarah Palin,[65] former US Senator Rick Santorum,[66] and Ann Coulter;[67] while New York Mayor Michael Bloomberg,[68] and the American Civil Liberties Union[69] publicly disagreed with Cathy's positions but defended his right to express them under the First Amendment.
Financial effect[edit]
Sales increased after the controversy. According to news coverage following the controversy:[70]
Chick-fil-A's sales soared 12 percent, to $4.6 billion, in 2012. The good fortune follows several years of impressive expansion and strong sales, which have pushed the privately held company's valuation north of $4.5 billion, making billionaires out of its founders ... These latest sales data are just further proof that all that negative coverage didn't hurt demand for chicken sandwiches among Chick-fil-A's core consumers.
—  Joe Satran, The Huffington Post
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text:
Atrial natriuretic peptide
From Wikipedia, the free encyclopedia
Jump to: navigation, search
For other uses, see ANP.
NPPA
Available structures
PDB
Ortholog search: PDBe RCSB
[show]List of PDB id codes
1ANP, 1YK0, 3N57
Identifiers
Aliases
NPPA, ANF, ANP, ATFB6, ATRST2, CDD, CDD-ANF, CDP, PND, Atrial natriuretic peptide, natriuretic peptide A
External IDs
OMIM: 108780 MGI: 97367 HomoloGene: 4498 GeneCards: NPPA
[hide]Gene location (Human)
Chr.
Chromosome 1 (human)[1]
Band
1p36.22
Start
11,845,709 bp[1]
End
11,848,345 bp[1]
[show]Gene location (Mouse)
Chr.
Chromosome 4 (mouse)[2]
Band
4 E2|4 78.66 cM
Start
148,000,722 bp[2]
End
148,002,079 bp[2]
[show]Gene ontology
Molecular function
• neuropeptide receptor binding
• hormone activity
• peptide hormone receptor binding
• neuropeptide hormone activity
• protein binding
• receptor binding
• hormone receptor binding
Cellular component
• cytoplasm
• mast cell granule
• nucleus
• perinuclear region of cytoplasm
• extracellular region
• extracellular space
• protein complex
• extracellular matrix
Biological process
• response to muscle stretch
• positive regulation of cardiac muscle contraction
• response to hypoxia
• regulation of high voltage-gated calcium channel activity
• neuropeptide signaling pathway
• female pregnancy
• regulation of cardiac conduction
• negative regulation of collecting lymphatic vessel constriction
• positive regulation of potassium ion export across plasma membrane
• cellular protein metabolic process
• regulation of blood vessel size
• positive regulation of heart rate
• positive regulation of delayed rectifier potassium channel activity
• cGMP biosynthetic process
• regulation of blood pressure
• negative regulation of systemic arterial blood pressure
• regulation of calcium ion transmembrane transport via high voltage-gated calcium channel
• transcription initiation from RNA polymerase II promoter
• regulation of atrial cardiac muscle cell membrane repolarization
• response to insulin
• cell growth involved in cardiac muscle cell development
• negative regulation of cell growth
• cardiac muscle hypertrophy in response to stress
• cellular response to mechanical stimulus
• receptor guanylyl cyclase signaling pathway
• protein folding
• regulation of receptor activity
• positive regulation of histamine secretion by mast cell
Sources:Amigo / QuickGO
Orthologs
Species
Human Mouse
Entrez
4878
230899
Ensembl
ENSG00000175206
ENSMUSG00000041616
UniProt
P01160
P05125
RefSeq (mRNA)
NM_006172
NM_008725
RefSeq (protein)
NP_006163
NP_032751
Location (UCSC)
Chr 1: 11.85 – 11.85 Mb Chr 1: 148 – 148 Mb
PubMed search
[3] [4]
Wikidata
View/Edit Human View/Edit Mouse
Atrial natriuretic peptide (ANP) is a peptide hormone which reduces an expanded extracellular fluid (ECF) volume by increasing renal sodium excretion. ANP is synthesized, and secreted by cardiac muscle cells in the walls of the atria in the heart. These cells contain volume receptors which respond to increased stretching of the atrial wall due to increased atrial blood volume. ANP is one of a family of nine natriuretic peptides: seven are atrial in origin.
ANP acts on the kidney to increase sodium and water excretion (natriuresis) in the following ways: 1) it dilates the glomerular afferent and constrict efferent arterioles, and relaxes the mesangial cells. This increases pressure in the glomerular capillaries, increasing the glomerular filtration rate (GFR), resulting in an increased amount of sodium and water being filtered and excreted. 2) It increases blood flow through the vasa recta, which washes the solutes sodium chloride (NaCl) and urea out of the medullary interstitium – the lower osmolarity here leads to less reabsorption of tubular fluid and increased excretion. 3) It decreases sodium reabsorption in the distal convoluted tubule and cortical collecting duct. 4) It inhibits renin secretion, thereby inhibiting the production of angiotensin and aldosterone. 5) It inhibits the renal sympathetic nervous system. ANP has the opposite effect of aldosterone on the kidney: aldosterone increases renal sodium retention and ANP increases renal sodium loss.[5][6]
Reduction of blood volume by ANP can result in secondary effects such as reduction of extracellular fluid (ECF) volume (edema), improved cardiac ejection fraction with resultant improved organ perfusion, decreased blood pressure, and increased serum potassium. These effects may be blunted or negated by various counter-regulatory mechanisms operating concurrently on each of these secondary effects.
Brain natriuretic peptide (BNP) – a misnomer; it is secreted by cardiac muscle cells in the heart ventricles – is similar to ANP in its effect. It acts via the same receptors as ANP does, but with 10-fold lower affinity than ANP. The biological half-life of BNP, however, is twice as long as that of ANP, and that of NT-proBNP is even longer, making these peptides better choices than ANP for diagnostic blood testing.
Contents
[hide]
1 Discovery
2 Structure
3 Production
4 Receptors
5 Physiological effects
5.1 Renal
5.2 Adrenal
5.3 Vascular
5.4 Cardiac
5.5 Adipose tissue
6 Degradation
7 Biomarker
8 Therapeutic use and drug development
9 Other natriuretic peptides
10 Pharmacological modulation
11 Synonyms
12 Outside reading
13 References
14 External links
Discovery[edit]
The discovery of ANP was reported in 1981, when rat atrial extracts were found to contain a substance that increased salt and urine output in the kidney.[7] Later, the substance was purified from heart tissue by several groups and named atrial natriuretic factor (ANF) or ANP.[8]
Structure[edit]
ANP is a 28-amino acid peptide with a 17-amino acid ring in the middle of the molecule. The ring is formed by a disulfide bond between two cysteine residues at positions 7 and 23. ANP is closely related to BNP (brain natriuretic peptide) and CNP (C-type natriuretic peptide), which all share a similar amino acid ring structure. ANP is one of a family of nine structurally similar natriuretic hormones: seven are atrial in origen.[9]
Production[edit]
Human ANP is encoded by the NPPA gene on the short arm of chromosome 1, which has 3 exons and 2 introns. The gene is expressed primarily in atrial myocytes. Lower levels of NPPA expression are found in other tissues such as the brain, kidney, lung, uterus and placenta.
In atrial myocytes, ANP is made as a precursor form, i.e. prepro-ANP, a polypeptide of 151 amino acids. After the signal peptide is removed in the endoplasmic reticulum, the 126-amino-acid pro-ANP is stored in the intracellular granules. When the cells are stimulated, pro-ANP is released and converted to the 28-amino-acid C-terminal mature ANP on the cell surface by the cardiac transmembrane serine protease corin.[10][11]
ANP is secreted in response to:
Stretching of the atrial wall, via Atrial volume receptors
Increased Sympathetic stimulation of β-adrenoceptors
Increased sodium concentration (hypernatremia), though sodium concentration is not the direct stimulus for increased ANP secretion[12]
Endothelin, a potent vasoconstrictor
Receptors[edit]
Three types of atrial natriuretic peptide receptors have been identified on which natriuretic peptides act. They are all cell surface receptors and designated:
guanylyl cyclase-A (GC-A) also known as natriuretic peptide receptor-A (NPRA/ANPA) or NPR1
guanylyl cyclase-B (GC-B) also known as natriuretic peptide receptor-B (NPRB/ANPB) or NPR2
natriuretic peptide clearance receptor (NPRC/ANPC) or NPR3
NPR-A and NPR-B have a single membrane-spanning segment with an extracellular domain that binds the ligand. The intracellular domain maintains two consensus catalytic domains for guanylyl cyclase activity. Binding of a natriuretic peptide induces a conformational change in the receptor that causes receptor dimerization and activation.
The binding of ANP to its receptor causes the conversion of GTP to cGMP and raises intracellular cGMP. As a consequence, cGMP activates a cGMP-dependent kinase (PKG or cGK) that phosphorylates proteins at specific serine and threonine residues. In the medullary collecting duct, the cGMP generated in response to ANP may act not only through PKG but also via direct modulation of ion channels.[13]
NPR-C functions mainly as a clearance receptor by binding and sequestering ANP from the circulation. All natriuretic peptides are bound by the NPR-C.
Physiological effects[edit]
Maintenance of the ECF volume (space), and its subcompartment the vascular space, is crucial for survival. These compartments are maintained within a narrow range, despite wide variations in dietary sodium intake. There are three volume regulating systems: two salt saving systems, the renin angiotensin aldosterone system (RAAS) and the renal sympathetic system (RSS); and the salt excreting natriuretic peptide (NP) hormone system. When the vascular space contracts, the RAAS and RSS are "turned on" ; when the atria expand, NP's are "turned on". Each system also suppresses its counteracting system(s). NP's are made in cardiac, intestinal, renal, and adrenal tissue: ANP in one of a family of cardiac NP's: others at BNP, CNP, and DNP.[14]
ANP binds to a specific set of receptors – ANP receptors. Receptor-agonist binding causes the increase in renal sodium excretion, which results in a decreased ECF and blood volume. Secondary effects may be an improvement in cardiac ejection fraction and reduction of systemic blood pressure.
Renal[edit]
Dilates the afferent glomerular arteriole, constricts the efferent glomerular arteriole, and relaxes the mesangial cells. This increases pressure in the glomerular capillaries, thus increasing the glomerular filtration rate (GFR), resulting in greater filter load of sodium and water.
Increases blood flow through the vasa recta, which will wash the solutes (sodium chloride (NaCl), and urea) out of the medullary interstitium.[15] The lower osmolarity of the medullary interstitium leads to less reabsorption of tubular fluid and increased excretion.
Decreases sodium reabsorption in the distal convoluted tubule (interaction with NCC)[16] and cortical collecting duct of the nephron via guanosine 3',5'-cyclic monophosphate (cGMP) dependent phosphorylation of ENaC.
Its natriuretic effect is affected by dopamine and dopamine receptor D1 activity in vivo [17]
Inhibits renin secretion, thereby inhibiting the renin–angiotensin–aldosterone system.
Adrenal[edit]
Reduces aldosterone secretion by the zona glomerulosa of the adrenal cortex.
Vascular[edit]
Relaxes vascular smooth muscle in arterioles and venules by:
Membrane Receptor-mediated elevation of vascular smooth muscle cGMP
Inhibition of the effects of catecholamines
Promotes uterine spiral artery remodeling, which is important for preventing pregnancy-induced hypertension.[18]
Cardiac[edit]
Inhibits maladaptive cardiac hypertrophy
Re-expression of NPRA rescues the phenotype.
Adipose tissue[edit]
Increases the release of free fatty acids from adipose tissue. Plasma concentrations of glycerol and nonesterified fatty acids are increased by i.v. infusion of ANP in humans.
Activates adipocyte plasma membrane type A guanylyl cyclase receptors NPR-A
Increases intracellular cGMP levels that induce the phosphorylation of a hormone-sensitive lipase and perilipin A via the activation of a cGMP-dependent protein kinase-I (cGK-I)
Does not modulate cAMP production or PKA activity
Degradation[edit]
Modulation of the effects of ANP is achieved through gradual degradation of the peptide by the enzyme neutral endopeptidase (NEP). Recently, NEP inhibitors have been developed; however they have not yet been licensed. They may be clinically useful in treating congestive heart disease.
Biomarker[edit]
Fragments derived from the ANP precursor, including the signal peptide, N-terminal pro-ANP and ANP, have been detected in human blood.[19] ANP and related peptides are used as biomarkers for cardiovascular diseases such as stroke, coronary artery disease, myocardial infarction and heart failure.[20][21][22][23]
Large amounts of ANP secretion has been noted to cause electrolyte disturbances (hyponatremia) and polyuria. These indications can be a marker of a large atrial myxoma.[24]
Therapeutic use and drug development[edit]
Recombinant human ANP has been approved in Japan to treat patients with heart failure.[25]
As of 2017 a truncated form of ANP called ularitide was under development in Phase III trials for heart failure.[26]
Other natriuretic peptides[edit]
Brain natriuretic peptide (BNP) – a misnomer; it is secreted by ventricular myocytes – is similar to ANP in its effect. It acts via atrial natriuretic peptide receptors but with 10-fold lower affinity than ANP. The biological half-life of BNP, however, is twice as long as that of ANP, and that of NT-proBNP is even longer, making these peptides better choices than ANP for diagnostic blood testing.
In addition to the mammalian natriuretic peptides (ANP, BNP, CNP), other natriuretic peptides with similar structure and properties have been isolated elsewhere in the animal kingdom. A salmon natriuretic peptide known as salmon cardiac peptide has been described,[27] and dendroaspis natriuretic peptide (DNP) has been found in the venom of the green mamba, as well as an NP in a species of African snake.[28]
Beside these four, five additional natriuretic peptides have been identified: long-acting natriuretic peptide (LANP), vessel dilator, kaliuretic peptide, urodilatin, and adrenomedullin.[29]
Pharmacological modulation[edit]
Neutral endopeptidase (NEP) also known as neprilysin is the enzyme that metabolizes natriuretic peptides. Several inhibitors of NEP are currently being developed to treat disorders ranging from hypertension to heart failure. Most of them are dual inhibitors (NEP and ACE). In 2014, PARADIGM-HF study was published in NEJM. This study considered as a landmark study in treatment of heart failure. The study was double blinded; compared LCZ696 versus enalapril in patients with heart failure. The study showed lower all cause mortality, cardiovascular mortality and hospitalization in LCZ696 arm.[30] Omapatrilat (dual inhibitor of NEP and angiotensin-converting enzyme) developed by BMS did not receive FDA approval due to angioedema safety concerns. Other dual inhibitors of NEP with ACE/angiotensin receptor are (in 2003) being developed by pharmaceutical companies.[31]
Synonyms[edit]
ANP is also called atrial natriuretic factor (ANF), atrial natriuretic hormone (ANH), cardionatrine, cardiodilatin (CDD), and atriopeptin.
Outside reading[edit]
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4855512/
Vesely Chapter 39, Antinatriureic peptides, in Seldin and Giebisch’s The Kidney, Fifth Edition. DOI:https://dx.doi.org/10.1016/B978-0-12-381462-3.00037-9. 2013 Elsevier Inc.
References[edit]
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Jump up ^ de Bold AJ (Nov 1985). "Atrial natriuretic factor: a hormone produced by the heart". Science. 230 (4727): 767–70. Bibcode:1985Sci...230..767D. doi:10.1126/science.2932797. PMID 2932797.
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Jump up ^ Reeves WB, Andreoli TE (2008). "Chapter 31 – Sodium Chloride Transport in the Loop of Henle, Distal Convoluted Tubule, and Collecting Duct". In Giebisch GH, Alpern RA, Herbert SC, Seldin DW. Seldin and Giebisch's the kidney: physiology and pathophysiology. Amsterdam: Elsevier/Academic Press. doi:10.1016/B978-012088488-9.50034-6. ISBN 0-12-088488-7.
Jump up ^ Fernandes-Cerqueira C, Sampaio-Maia B, Quelhas-Santos J, Moreira-Rodrigues M, Simões-Silva L, Blazquez-Medela AM, Martinez-Salgado C, Lopez-Novoa JM, Pestana M (2013). "Concerted action of ANP and dopamine D1-receptor to regulate sodium homeostasis in nephrotic syndrome". BioMed Research International. 2013: 397391. doi:10.1155/2013/397391. PMC 3727124  . PMID 23956981.
Jump up ^ Cui Y, Wang W, Dong N, Lou J, Srinivasan DK, Cheng W, Huang X, Liu M, Fang C, Peng J, Chen S, Wu S, Liu Z, Dong L, Zhou Y, Wu Q (Apr 2012). "Role of corin in trophoblast invasion and uterine spiral artery remodelling in pregnancy". Nature. 484 (7393): 246–50. Bibcode:2012Natur.484..246C. doi:10.1038/nature10897. PMC 3578422  . PMID 22437503.
Jump up ^ Goetze JP, Hansen LH, Terzic D, Zois NE, Albrethsen J, Timm A, Smith J, Soltysinska E, Lippert SK, Hunter I (Mar 2015). "Atrial natriuretic peptides in plasma". Clinica Chimica Acta; International Journal of Clinical Chemistry. 443: 25–8. doi:10.1016/j.cca.2014.08.017. PMID 25158019.
Jump up ^ Wang TJ, Larson MG, Levy D, Benjamin EJ, Leip EP, Omland T, Wolf PA, Vasan RS (Feb 2004). "Plasma natriuretic peptide levels and the risk of cardiovascular events and death". The New England Journal of Medicine. 350 (7): 655–63. doi:10.1056/NEJMoa031994. PMID 14960742.
Jump up ^ Sabatine MS, Morrow DA, de Lemos JA, Omland T, Sloan S, Jarolim P, Solomon SD, Pfeffer MA, Braunwald E (Jan 2012). "Evaluation of multiple biomarkers of cardiovascular stress for risk prediction and guiding medical therapy in patients with stable coronary disease". Circulation. 125 (2): 233–40. doi:10.1161/CIRCULATIONAHA.111.063842. PMC 3277287  . PMID 22179538.
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Jump up ^ Barbato E, Bartunek J, Marchitti S, Mangiacapra F, Stanzione R, Delrue L, Cotugno M, Di Castro S, De Bruyne B, Wijns W, Volpe M, Rubattu S (Mar 2012). "NT-proANP circulating level is a prognostic marker in stable ischemic heart disease". International Journal of Cardiology. 155 (2): 311–2. doi:10.1016/j.ijcard.2011.11.057. PMID 22177588.
Jump up ^ Ramnarain, D; Mehra, N (2011). "Natriuretic peptide-induced hyponatremia in a patient with left atrial myxoma". Critical Care. 15 (Suppl 1): P368. doi:10.1186/cc9788. PMC 3067042  .
Jump up ^ Saito Y (Nov 2010). "Roles of atrial natriuretic peptide and its therapeutic use". Journal of Cardiology. 56 (3): 262–70. doi:10.1016/j.jjcc.2010.08.001. PMID 20884176.
Jump up ^ "Ularitide". AdisInsight. Retrieved 6 August 2017.
Jump up ^ Tervonen V, Arjamaa O, Kokkonen K, Ruskoaho H, Vuolteenaho O (Sep 1998). "A novel cardiac hormone related to A-, B- and C-type natriuretic peptides". Endocrinology. 139 (9): 4021–5. doi:10.1210/en.139.9.4021. PMID 9724061.
Jump up ^ Schweitz H, Vigne P, Moinier D, Frelin C, Lazdunski M (Jul 1992). "A new member of the natriuretic peptide family is present in the venom of the green mamba (Dendroaspis angusticeps)". The Journal of Biological Chemistry. 267 (20): 13928–32. PMID 1352773.
Jump up ^ Vesely Chapter 39, Antinatriureic peptides, in Seldin and Giebisch’s The Kidney, Fifth Edition. DOI:https://dx.doi.org/10.1016/B978-0-12-381462-3.00037-9. (c)2013 Elsevier Inc.
Jump up ^ McMurray JJ, Packer M, Desai AS, Gong J, Lefkowitz MP, Rizkala AR, Rouleau JL, Shi VC, Solomon SD, Swedberg K, Zile MR (Sep 2014). "Angiotensin-neprilysin inhibition versus enalapril in heart failure". The New England Journal of Medicine. 371 (11): 993–1004. doi:10.1056/NEJMoa1409077. PMID 25176015.
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External links[edit]
Atrial Natriuretic Factor at the US National Library of Medicine Medical Subject Headings (MeSH)
Human NPPA genome location and NPPA gene details page in the UCSC Genome Browser.
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values: ببتيد أذيني مدر للصوديوم – Arabic

values: Atriales natriuretisches Peptid – German

values: އެޓްރީއަލް ނެޓްރީޔުރެޓިކް ޕެޕްޓައިޑް – Divehi

values: Péptido natriurético auricular – Spanish

values: Facteur natriurétique auriculaire – French

values: Peiptíd aitriach shóidiambhrostach – Irish

values: Péptido natriurético auricular – Galician

values: 심방 나트륨이뇨 펩티드 – Korean

values: Նատրիումամուղ հորմոն – Armenian

values: Атријален натриуретичен пептид – Macedonian

values: 心房性ナトリウム利尿ペプチド – Japanese

values: Przedsionkowy peptyd natriuretyczny – Polish

values: Peptídeo natriurético atrial – Portuguese

values: Предсердный натрийуретический пептид – Russian

values: Atrial-natriuretic peptide – Simple English

values: Atrijski natriuretični peptid – Slovenian

values: A-tyypin natriureettinen peptidi – Finnish

values: இதயியச் சோடியச்சிறுநீர்மைப் புரதக்கூறு – Tamil

values: Передсердний натрійуретичний фактор – Ukrainian

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Common carotid artery
From Wikipedia, the free encyclopedia
Jump to: navigation, search
"Carotids" redirects here. For the parotids (salivary glands), see Parotid gland.
Common carotid artery
The common carotid artery arises directly from the aorta on the left, and as a branch of the brachiocephalic trunk on the right
The common carotid artery and its main branches
Details
Precursor
aortic arch 3
Source
aortic arch, brachiocephalic artery
Branches
internal carotid artery, external carotid artery
Vein
internal jugular vein
Supplies
head and neck
Identifiers
Latin
Arteria carotis communis
MeSH
A07.231.114.186.200
Dorlands
/Elsevier
a_61/12153659
TA
A12.2.04.006
FMA
3939
Anatomical terminology
[edit on Wikidata]
In anatomy, the left and right common carotid arteries (English: /kəˈrɒtɪd/[1][2]) are arteries that supply the head and neck with oxygenated blood; they divide in the neck to form the external and internal carotid arteries.[3][4]
Contents
[hide]
1 Structure
1.1 In the chest
1.2 In the neck
2 Collateral circulation
3 Variation
3.1 Origin
3.2 Point of division
3.3 Occasional branches
4 Clinical significance
5 Gallery
6 See also
7 References
8 External links
Structure[edit]
The common carotid arteries are present on the left and right sides of the body. These arteries originate from different arteries, but follow symmetrical courses. The right common carotid originates in the neck from the brachiocephalic trunk; the left from the aortic arch in the thorax. These split into the external and internal carotid arteries at the upper border of the thyroid cartilage, at around the level of the fourth cervical vertebra.
The left common carotid artery can be thought of as having two parts: a thoracic (chest) part and a cervical (neck) part. The right common carotid originates in or close to the neck, so contains only a small thoracic portion. There are studies in the bioengineering literature that have looked into characterizing the geometric structure of the common carotid artery from both qualitative and mathematical (quantitative) standpoints.[4]
The average diameters of the common carotids in adult males and females are 6.5 mm and 6.1 mm respectively.[5]
In the chest[edit]
Only the left common carotid artery has a substantial presence in the thorax. It originates directly from the aortic arch, and travels upward through the superior mediastinum to the level of the left sternoclavicular joint.
During the thoracic part of its course, the left common carotid artery is related to the following structures: In front, it is separated from the manubrium of the sternum by the sternohyoid and sternothyroid muscles, the anterior portions of the left pleura and lung, the left brachiocephalic vein, and the remains of the thymus; behind, it lies on the trachea, esophagus, left recurrent laryngeal nerve, and thoracic duct.
To its right side below is the brachiocephalic trunk, and above, the trachea, the inferior thyroid veins, and the remains of the thymus; to its left side are the left vagus and phrenic nerves, left pleura, and lung. The left subclavian artery is posterior and slightly lateral to it.
In the neck[edit]
Arteries of the neck. The right common carotid artery – labeled Common caroti in the figure – divides into the right internal carotid artery and external carotid artery.
The cervical portions of the common carotids resemble each other so closely that one description will apply to both.
Each vessel passes obliquely upward, from behind the sternoclavicular joint to the level of the upper border of the thyroid cartilage, where it divides.
At the lower neck the two common carotid arteries are separated from each other by a very narrow interval which contains the trachea; but at the upper part, the thyroid gland, the larynx and pharynx separate the two arteries.
The common carotid artery is contained in a sheath known as the carotid sheath, which is derived from the deep cervical fascia and encloses also the internal jugular vein and vagus nerve, the vein lying lateral to the artery, and the nerve between the artery and vein, on a plane posterior to both. On opening the sheath, each of these three structures is seen to have a separate fibrous cover.
At approximately the level of the fourth cervical vertebra, the common carotid artery splits ("bifurcates" in literature) into an internal carotid artery (ICA) and an external carotid artery (ECA). While both branches travel upward, the internal carotid takes a deeper (more internal) path, eventually travelling up into the skull to supply the brain. The external carotid artery travels more closely to the surface, and sends off numerous branches that supply the neck and face.
Superficial dissection of the right side of the neck, showing the carotid and subclavian arteries.
At the lower part of the neck the common carotid artery is very deeply seated, being covered by the integument, superficial fascia, the platysma muscle, deep cervical fascia, the sternocleidomastoid muscle, the sternohyoid, sternothyroid, and the omohyoid; in the upper part of its course it is more superficial, being covered merely by the integument, the superficial fascia, the platysma, deep cervical fascia, and medial margin of the sternocleidomastoid.
When the sternocleidomastoid muscle is drawn backward, the artery is seen to be contained in a triangular space known as the carotid triangle. This space is bounded behind by the sternocleidomastoid, above by the stylohyoid and the posterior belly of the digastric muscle, and below by the superior belly of the omohyoid.
This part of the artery is crossed obliquely, from its medial to its lateral side, by the sternocleidomastoid branch of the superior thyroid artery; it is also crossed by the superior and middle thyroid veins (which end in the internal jugular vein); descending in front of its sheath is the descending branch of the hypoglossal nerve, this filament being joined by one or two branches from the cervical nerves, which cross the vessel obliquely.
Sometimes the descending branch of the hypoglossal nerve is contained within the sheath.
The superior thyroid vein crosses the artery near its termination, and the middle thyroid vein a little below the level of the cricoid cartilage; the anterior jugular vein crosses the artery just above the clavicle, but is separated from it by the sternohyoid and sternothyroid.
Behind, the artery is separated from the transverse processes of the cervical vertebrae by the longus colli and longus capitis muscles, the sympathetic trunk being interposed between it and the muscles. The inferior thyroid artery crosses behind the lower part of the vessel.
Medially, it is in relation with the esophagus, trachea, and thyroid gland (which overlaps it), the inferior thyroid artery and recurrent laryngeal nerve being interposed; higher up, with the larynx and pharynx. Lateral to the artery, inside the carotid sheath with the common carotid, are the internal jugular vein and vagus nerve.
At the lower part of the neck, on the right side of the body, the right recurrent laryngeal nerve crosses obliquely behind the artery; the right internal jugular vein diverges from the artery. On the left side, however, the left internal jugular vein approaches and often overlaps the lower part of the artery.
Behind the angle of bifurcation of the common carotid artery is a reddish-brown oval body known as the carotid body. It is similar in structure to the coccygeal body which is situated on the median sacral artery.
The relations of the cervical region of the common carotid artery may be discussed in two points:
Internal relations of organs present inside the carotid sheath
two external relations of carotid sheath
Collateral circulation[edit]
After ligature of the common carotid, the collateral circulation can be perfectly established, by the free communication which exists between the carotid arteries of opposite sides, both without and within the cranium, and by enlargement of the branches of the subclavian artery on the side corresponding to that on which the vessel has been tied.
The chief communications outside the skull take place between the superior and inferior thyroid arteries, and the deep cervical artery and the descending branch of the occipital artery; the vertebral artery takes the place of the internal carotid artery within the cranium.
Variation[edit]
Origin[edit]
The right common carotid may arise above the level of the upper border of the sternoclavicular joint; this variation occurs in about 12 percent of cases.
In other cases the artery on the right side may arise as a separate branch from the arch of the aorta, or in conjunction with the left carotid.
The left common carotid varies in its origin more than the right.
In the majority of abnormal cases it arises with the brachiocephalic trunk; if that artery is absent, the two carotids arise usually by a single trunk.
It is rarely joined with the left subclavian artery, except in cases of transposition of the aortic arch.
Point of division[edit]
In the majority of abnormal cases, the bifurcation occurs higher than usual, the artery dividing opposite or even above the hyoid bone; more rarely, it occurs below, opposite the middle of the larynx, or the lower border of the cricoid cartilage. In at least one reported case, the artery was only 4 cm in length and divided at the root of the neck.
Very rarely, the common carotid artery ascends in the neck without any subdivision, either the external or the internal carotid being absent; and in a few cases the common carotid has itself been found to be absent, the external and internal carotids arising directly from the arch of the aorta.
This peculiarity existed on both sides in some instances, on one side in others.
Occasional branches[edit]
The common carotid usually gives off no branch previous to its bifurcation, but it occasionally gives origin to the superior thyroid artery or its laryngeal branch, the ascending pharyngeal artery, the inferior thyroid artery, or, more rarely, the vertebral artery.
Clinical significance[edit]
The common carotid artery is often used in measuring the pulse,[3] especially in patients who are in shock and who lack a detectable pulse in the more peripheral arteries of the body. The pulse is taken by palpating the artery just deep to the anterior border of the sternocleidomastoid muscle at the level of the superior border of the thyroid cartilage.
Presence of a carotid pulse has been estimated to indicate a systolic blood pressure of more than 40 mmHg, as given by the 50% percentile.[6]
Carotidynia is a syndrome marked by soreness of the carotid artery near the bifurcation.
Carotid stenosis may occur in patients with atherosclerosis.
The intima-media thickness of the carotid artery wall is a marker of subclinical atherosclerosis, it increases with age and with long-term exposure to particulate air pollution. [7]
Gallery[edit]
Magnetic Resonance Angiography
Normal carotidal arteriography
Common carotid artery
Common carotid artery – right view
Brachial plexus and common carotid artery
Common carotid artery
Common carotid artery
Right and left common carotid arteries
See also[edit]
Head and neck anatomy
Carotid sheath
Carotid sinus
Carotid body
Carotid Doppler machine
Carotidynia
References[edit]
Jump up ^ OED 2nd edition, 1989.
Jump up ^ Entry "carotid" in Merriam-Webster Online Dictionary.
^ Jump up to: a b Ashrafian H. Anatomically specific clinical examination of the carotid arterial tree. Anat Sci Int. 2007 Mar;82(1):16–23.
^ Jump up to: a b Manbachi, A., Hoi, Y., Wasserman, B. A. Lakatta, E.G. and Steinman. D.A. (November 2011). "On the shape of the common carotid artery with implications for blood velocity profiles.". Physiol. Meas. 32 (12): 1885–1897. PMC 3494738  . PMID 22031538. doi:10.1088/0967-3334/32/12/001. CS1 maint: Multiple names: authors list (link)
Jump up ^ J. Krejza; M. Arkuszewski; S. Kasner; J. Weigele; A. Ustymowicz; R. Hurst; B. Cucchiara; S. Messe (April 2006). "Carotid Artery Diameter in Men and Women and the Relation to Body and Neck Size.". Stroke. 37 (4): 1103–1105. PMID 16497983. doi:10.1161/01.STR.0000206440.48756.f7.
Jump up ^ Deakin CD, Low JL (September 2000). "Accuracy of the advanced trauma life support guidelines for predicting systolic blood pressure using carotid, femoral, and radial pulses: observational study". BMJ. 321 (7262): 673–4. PMC 27481  . PMID 10987771. doi:10.1136/bmj.321.7262.673.
Jump up ^ Provost, E; Madhloum, N; Int Panis, L; De Boever, P; Nawrot, T (2015). "Carotid Intima-Media Thickness, a Marker of Subclinical Atherosclerosis, and Particulate Air Pollution Exposure: the Meta-Analytical Evidence". PLOS ONE. 10 (5): e0127014. PMC 4430520  . PMID 25970426. doi:10.1371/journal.pone.0127014.
External links[edit]
Wikimedia Commons has media related to Common carotid artery.
Anatomy figure: 21:06-01 at Human Anatomy Online, SUNY Downstate Medical Center
Blood flow numerical simulations in stenosed carotid
[hide]
v
t
e
Arteries of the torso and chest
Lungs
Pulmonary artery
Right
Left (Ligamentum arteriosum)
Heart
Coronary circulation
Right coronary:
SA nodal
AV nodal
Atrial
Right marginal
Posterior interventricular
Left coronary:
Anterior interventricular
Left circumflex (Left marginal)
Aorta
Sections
Ascending aorta
Aortic arch
Descending aorta
Thoracic aorta
Abdominal aorta
Aortic body
Aortic arch
Brachiocephalic
Thyreoidea ima
Right subclavian
Right common carotid
Left
common carotid
External carotid
Internal carotid
Carotid body
Carotid sinus
Carotid bifurcation
Left
subclavian
Internal thoracic: Anterior intercostal
Thymic
Pericardiacophrenic
Perforating branches
terminal (Musculophrenic, superior epigastric)
Costocervical trunk: Highest intercostal (Posterior intercostal 1–2)
Deep cervical
Descending
aorta
visceral: Bronchial
Esophageal
Mediastinal
parietal: Posterior intercostal 3–11
Subcostal
Superior phrenic
Retrieved from "https://en.wikipedia.org/w/index.php?title=Common_carotid_artery&oldid=794999297"
Categories:
Arteries of the head and neck
Arteries of the thorax
Hidden categories:
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