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Aldosterone
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Aldosterone
Names
IUPAC name
11β,21-Dihydroxy-3,20-dioxopregn-4-en-18-al
Identifiers
CAS Number
52-39-1 Y
3D model (JSmol)
Interactive image
ChEBI
CHEBI:27584 Y
ChEMBL
ChEMBL273453 Y
ChemSpider
5633 Y
DrugBank
DB04630 Y
ECHA InfoCard 100.000.128
IUPHAR/BPS
2872
KEGG
D10528 N
MeSH Aldosterone
PubChem CID
5839
InChI[show]
InChI=1S/C21H28O5/c1-20-7-6-13(24)8-12(20)2-3-14-15-4-5-16(18(26)10-22)21(15,11-23)9-17(25)19(14)20/h8,11,14-17,19,22,25H,2-7,9-10H2,1H3/t14-,15-,16+,17-,19+,20-,21+/m0/s1 Y
Key: PQSUYGKTWSAVDQ-ZVIOFETBSA-N Y
InChI=1/C21H28O5/c1-20-7-6-13(24)8-12(20)2-3-14-15-4-5-16(18(26)10-22)21(15,11-23)9-17(25)19(14)20/h8,11,14-17,19,22,25H,2-7,9-10H2,1H3/t14-,15-,16+,17-,19+,20-,21+/m0/s1
Key: PQSUYGKTWSAVDQ-ZVIOFETBBV
SMILES[show]
O=C(CO)[C@@H]4[C@@]3(C=O)C[C@H](O)[C@@H]2[C@@]1(/C(=C\C(=O)CC1)CC[C@H]2[C@@H]3CC4)C
Properties
Chemical formula
C21H28O5
Molar mass 360.45 g·mol−1
Pharmacology
ATC code
H02AA01 (WHO)
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
N verify (what is Y N ?)
Infobox references
Aldosterone, the main mineralocorticoid hormone, is a steroid hormone produced by the zona glomerulosa of the adrenal cortex in the adrenal gland.[1][2] It is essential for sodium conservation in the kidney, salivary glands, sweat glands and colon.[3] It plays a central role in the homeostatic regulation of blood pressure, plasma sodium (Na+), and potassium (K+) levels. It does so mainly by acting on the mineralocorticoid receptors in the distal tubules and collecting ducts of the nephron.[3] It influences the reabsorption of sodium and excretion of potassium (from and into the tubular fluids, respectively) of the kidney, thereby indirectly influencing water retention or loss, blood pressure and blood volume.[4] When dysregulated, aldosterone is pathogenic and contributes to the development and progression of cardiovascular and renal disease.[5] Aldosterone has exactly the opposite function of the atrial natriuretic hormone secreted by the heart.[4]
Aldosterone is part of the renin–angiotensin–aldosterone system. It has a plasma half-life of under 20 minutes.[6] Drugs that interfere with the secretion or action of aldosterone are in use as antihypertensives, like lisinopril, which lowers blood pressure by blocking the angiotensin-converting enzyme (ACE), leading to lower aldosterone secretion. The net effect of these drugs is to reduce sodium and water retention but increase retention of potassium. In other words, these drugs stimulate the excretion of sodium and water in urine, while they block the excretion of potassium.
Another example is spironolactone, a potassium-sparing diuretic of the steroidal spirolactone group, which decreases blood pressure by releasing fluid from the body while retaining potassium.
Aldosterone was first isolated by Simpson and Tait in 1953.[7]
Contents
[hide]
1 Biosynthesis
1.1 Stimulation
2 Biological function
3 Mineralocorticoid receptors
4 Control of aldosterone release from the adrenal cortex
4.1 Major regulators
4.1.1 The role of the renin–angiotensin system
4.1.2 The plasma concentration of potassium
4.1.3 Adrenocorticotropic hormone
4.2 Miscellaneous regulators
4.2.1 The role of sympathetic nerves
4.2.2 The role of baroreceptors
4.2.3 The plasma concentration of sodium
4.3 Aldosterone feedback
5 Associated clinical conditions
5.1 Hyperaldosteronism
5.2 Hypoaldosteronism
6 Additional images
7 See also
8 References
9 External links
Biosynthesis[edit]
The corticosteroids are synthesized from cholesterol within the zona glomerulosa of adrenal cortex. Most steroidogenic reactions are catalysed by enzymes of the cytochrome P450 family. They are located within the mitochondria and require adrenodoxin as a cofactor (except 21-hydroxylase and 17α-hydroxylase).
Aldosterone and corticosterone share the first part of their biosynthetic pathways. The last parts are mediated either by the aldosterone synthase (for aldosterone) or by the 11β-hydroxylase (for corticosterone). These enzymes are nearly identical (they share 11β-hydroxylation and 18-hydroxylation functions), but aldosterone synthase is also able to perform an 18-oxidation. Moreover, aldosterone synthase is found within the zona glomerulosa at the outer edge of the adrenal cortex; 11β-hydroxylase is found in the zona glomerulosa and zona fasciculata.
Steroidogenesis, showing aldosterone synthesis at upper-right corner.[8]
Note: aldosterone synthase is absent in other sections of the adrenal gland.
Stimulation[edit]
Aldosterone synthesis is stimulated by several factors:
increase in the plasma concentration of angiotensin III, a metabolite of angiotensin II
increase in plasma angiotensin II, ACTH, or potassium levels, which are present in proportion to plasma sodium deficiencies. (The increased potassium level works to regulate aldosterone synthesis by depolarizing the cells in the zona glomerulosa, which opens the voltage-dependent calcium channels.) The level of angiotensin II is regulated by angiotensin I, which is in turn regulated by renin, a hormone secreted in the kidneys.
Serum potassium concentrations are the most potent stimulator of aldosterone secretion.
the ACTH stimulation test, which is sometimes used to stimulate the production of aldosterone along with cortisol to determine whether primary or secondary adrenal insufficiency is present. However, ACTH has only a minor role in regulating aldosterone production; with hypopituitarism there is no atrophy of the zona glomerulosa.
plasma acidosis
the stretch receptors located in the atria of the heart. If decreased blood pressure is detected, the adrenal gland is stimulated by these stretch receptors to release aldosterone, which increases sodium reabsorption from the urine, sweat, and the gut. This causes increased osmolarity in the extracellular fluid, which will eventually return blood pressure toward normal.
adrenoglomerulotropin, a lipid factor, obtained from pineal extracts. It selectively stimulates secretion of aldosterone.[9]
The secretion of aldosterone has a diurnal rhythm.[10]
Biological function[edit]
Aldosterone is the primary of several endogenous members of the class of mineralocorticoids in humans. Deoxycorticosterone is another important member of this class. Aldosterone tends to promote Na+ and water retention, and lower plasma K+ concentration by the following mechanisms:
Acting on the nuclear mineralocorticoid receptors (MR) within the principal cells of the distal tubule and the collecting duct of the kidney nephron, it upregulates and activates the basolateral Na+/K+ pumps, which pumps three sodium ions out of the cell, into the interstitial fluid and two potassium ions into the cell from the interstitial fluid. This creates a concentration gradient which results in reabsorption of sodium (Na+) ions and water (which follows sodium) into the blood, and secreting potassium (K+) ions into the urine (lumen of collecting duct).
Aldosterone upregulates epithelial sodium channels (ENaCs) in the collecting duct and the colon, increasing apical membrane permeability for Na+ and thus absorption.
Cl− is reabsorbed in conjunction with sodium cations to maintain the system's electrochemical balance.
Aldosterone stimulates the secretion of K+ into the tubular lumen.[11]
Aldosterone stimulates Na+ and water reabsorption from the gut, salivary and sweat glands in exchange for K+.
Aldosterone stimulates secretion of H+ via the H+/ATPase in the intercalated cells of the cortical collecting tubules
Aldosterone upregulates expression of NCC in the distal convoluted tubule chronically and its activity acutely.[12]
Aldosterone is responsible for the reabsorption of about 2% of filtered sodium in the kidneys, which is nearly equal to the entire sodium content in human blood under normal glomerular filtration rates.[13]
Aldosterone, probably acting through mineralocorticoid receptors, may positively influence neurogenesis in the dentate gyrus.[14]
Mineralocorticoid receptors[edit]
Steroid receptors are intracellular. The aldosterone mineralocorticoid receptor (MR) complex binds on the DNA to specific hormone response element, which leads to gene specific transcription. Some of the transcribed genes are crucial for transepithelial sodium transport, including the three subunits of the epithelial sodium channel (ENaC), the Na+/K+ pumps and their regulatory proteins serum and glucocorticoid-induced kinase, and channel-inducing factor, respectively.
The MR is stimulated by both aldosterone and cortisol, but a mechanism protects the body from excess aldosterone receptor stimulation by glucocorticoids (such as cortisol), which happen to be present at much higher concentrations than mineralocorticoids in the healthy individual. The mechanism consists of an enzyme called 11 β-hydroxysteroid dehydrogenase (11β-HSD). This enzyme co-localizes with intracellular adrenal steroid receptors and converts cortisol into cortisone, a relatively inactive metabolite with little affinity for the MR. Liquorice, which contains glycyrrhetinic acid, can inhibit 11β-HSD and lead to a mineralocorticoid excess syndrome.
Control of aldosterone release from the adrenal cortex[edit]
The renin–angiotensin system, showing role of aldosterone between the adrenal glands and the kidneys[15]
Major regulators[edit]
The role of the renin–angiotensin system[edit]
Angiotensin is involved in regulating aldosterone and is the core regulation.[16] Angiotensin II acts synergistically with potassium, and the potassium feedback is virtually inoperative when no angiotensin II is present.[17] A small portion of the regulation resulting from angiotensin II must take place indirectly from decreased blood flow through the liver due to constriction of capillaries.[18] When the blood flow decreases so does the destruction of aldosterone by liver enzymes.
Although sustained production of aldosterone requires persistent calcium entry through low-voltage-activated Ca2+ channels, isolated zona glomerulosa cells are considered nonexcitable, with recorded membrane voltages that are too hyperpolarized to permit Ca2+ channels entry.[19] However, mouse zona glomerulosa cells within adrenal slices spontaneously generate membrane potential oscillations of low periodicity; this innate electrical excitability of zona glomerulosa cells provides a platform for the production of a recurrent Ca2+ channels signal that can be controlled by angiotensin II and extracellular potassium, the 2 major regulators of aldosterone production.[19] Voltage-gated Ca2+ channels have been detected in the zona glomerulosa of the human adrenal, which suggests that Ca2+ channel blockers may directly influence the adrenocortical biosynthesis of aldosterone in vivo.[20]
The plasma concentration of potassium[edit]
The amount of aldosterone secreted is a direct function of the serum potassium[21][22] as probably determined by sensors in the carotid artery.[23][24]
Adrenocorticotropic hormone[edit]
Adrenocorticotropic hormone (ACTH), a pituitary peptide, also has some stimulating effect on aldosterone, probably by stimulating the formation of deoxycorticosterone, a precursor of aldosterone.[25] Aldosterone is increased by blood loss,[26] pregnancy,[27] and possibly by further circumstances such as physical exertion, endotoxin shock, and burns.[28][29]
Miscellaneous regulators[edit]
The role of sympathetic nerves[edit]
The aldosterone production is also affected to one extent or another by nervous control, which integrates the inverse of carotid artery pressure,[23] pain, posture,[27] and probably emotion (anxiety, fear, and hostility)[30] (including surgical stress).[31] Anxiety increases aldosterone,[30] which must have evolved because of the time delay involved in migration of aldosterone into the cell nucleus.[32] Thus, there is an advantage to an animal's anticipating a future need from interaction with a predator, since too high a serum content of potassium has very adverse effects on nervous transmission.
The role of baroreceptors[edit]
Pressure-sensitive baroreceptors are found in the vessel walls of nearly all large arteries in the thorax and neck, but are particularly plentiful in the sinuses of the carotid arteries and in the arch of the aorta. These specialized receptors are sensitive to changes in mean arterial pressure. An increase in sensed pressure results in an increased rate of firing by the baroreceptors and a negative feedback response, lowering systemic arterial pressure. Aldosterone release causes sodium and water retention, which causes increased blood volume, and a subsequent increase in blood pressure, which is sensed by the baroreceptors.[33] To maintain normal homeostasis these receptors also detect low blood pressure or low blood volume, causing aldosterone to be released. This results in sodium retention in the kidney, leading to water retention and increased blood volume.[34]

The plasma concentration of sodium[edit]
Aldosterone is a function of the inverse of the sodium intake as sensed via osmotic pressure.[35] The slope of the response of aldosterone to serum potassium is almost independent of sodium intake.[36] Aldosterone is increased at low sodium intakes, but the rate of increase of plasma aldosterone as potassium rises in the serum is not much lower at high sodium intakes than it is at low. Thus, the potassium is strongly regulated at all sodium intakes by aldosterone when the supply of potassium is adequate, which it usually is in primitive diets.
Aldosterone feedback[edit]
Feedback by aldosterone concentration itself is of a nonmorphological character (that is, other than changes in the cells' number or structure) and is poor, so the electrolyte feedbacks predominate, short term.[28]
Associated clinical conditions[edit]
Hyperaldosteronism is abnormally increased levels of aldosterone, while hypoaldosteronism is abnormally decreased levels of aldosterone.
A measurement of aldosterone in blood may be termed a plasma aldosterone concentration (PAC), which may be compared to plasma renin activity (PRA) as an aldosterone-to-renin ratio.
Hyperaldosteronism[edit]
Primary aldosteronism, also known as primary hyperaldosteronism, is characterized by the overproduction of aldosterone by the adrenal glands,[37] when not a result of excessive renin secretion. It leads to arterial hypertension (high blood pressure) associated with hypokalemia, usually a diagnostic clue. Secondary hyperaldosteronism, on the other hand, is due to overactivity of the renin–angiotensin system.
Conn's syndrome is primary hyperaldosteronism caused by an aldosterone-producing adenoma.
Depending on cause and other factors, hyperaldosteronism can be treated by surgery and/or medically, such as by aldosterone antagonists.
Hypoaldosteronism[edit]
An ACTH stimulation test for aldosterone can help in determining the cause of hypoaldosteronism, with a low aldosterone response indicating a primary hypoaldosteronism of the adrenals, while a large response indicating a secondary hypoaldosteronism.
Additional images[edit]
Corticosteroid biosynthetic pathway in rat
Corticosterone
See also[edit]
Mineralocorticoid
References[edit]
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^ Jump up to: a b Gann DS Mills IH Bartter 1960 On the hemodynamic parameter mediating increase in aldosterone secretion in the dog. Fed. Proceedings 19; 605–610.
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External links[edit]
Aldosterone at Lab Tests Online
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Androstanes: 3α-Androstanediol
3α-Androstenol
7-Keto-DHEA
7α-Hydroxy-DHEA
7β-Hydroxy-DHEA
7α-Hydroxyepiandrosterone
7β-Hydroxyepiandrosterone
Androsterone
DHEA
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Etiocholanolone
Pheromones: 3α-Androstenol
3β-Androstenol
Androstadienol
Androstadienone
Androstenone
Androsterone
Estratetraenol
Others
Vitamin D: 7-Dehydrocholesterol
Calcidiol/Calcifediol
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Cholecalciferol
Others: 7α-Hydroxycholesterol
11α-Hydroxyprogesterone
11β-Hydroxyprogesterone
Cholesterol sulfate
[show]
v
t
e
Physiology of the kidneys and acid-base physiology
Renal function
Secretion
clearance
Pharmacokinetics
Clearance of medications
Urine flow rate
Reabsorption
Solvent drag
sodium
chloride
urea
glucose
oligopeptides
protein
Renal function
Glomerular filtration rate
Creatinine clearance
Renal clearance ratio
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Filtration
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Hormones
Antidiuretic hormone
Aldosterone
Atrial natriuretic peptide
Renin
Erythropoietin
Calcitriol
Prostaglandins
Acid-base balance
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Darrow Yannet diagram
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Extracellular fluid
(Interstitial fluid
Plasma
Transcellular fluid)
Base excess
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Winters' formula
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Respiratory compensation
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Other
Fractional sodium excretion
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Urine
[show]
v
t
e
Mineralocorticoids and antimineralocorticoids (H02)
Mineralocorticoids
Desoxycortone (desoxycorticosterone)
Desoxycortone esters
Hydrocortisone (cortisol)
Hydrocortisone esters
Fludrocortisone
Fludrocortisone acetate
Methylprednisolone
Methylprednisolone esters
Prednisolone
Prednisolone esters
Prednisone
Prednisone esters
Antimineralocorticoids
Steroidal: Canrenoate potassium (potassium canrenoate)
Canrenone
Drospirenone
Dydrogesterone
Eplerenone
Gestodene
Medrogestone
Progesterone
Spironolactone
Trimegestone
Nonsteroidal: Amlodipine
Apararenone§
Benidipine
Esaxerenone†
Felodipine
Finerenone†
Nifedipine
Nimodipine
Nitrendipine
Synthesis modifiers
Acetoxolone
Aminoglutethimide
Carbenoxolone
Enoxolone
Ketoconazole
Metyrapone
Mitotane
Trilostane
#WHO-EM
‡Withdrawn from market
Clinical trials:
†Phase III
§Never to phase III
See also
Mineralocorticoid receptor modulators
Glucocorticoids and antiglucocorticoids
List of corticosteroids
[show]
v
t
e
Mineralocorticoid receptor modulators
MR
Agonists
11-Dehydrocorticosterone (11-oxocorticosterone, 17-deoxycortisone)
11-Dehydrocorticosterone acetate
11-Deoxycorticosterone (desoxycortone, deoxycortone, desoxycorticosterone)
Desoxycortone esters
11-Deoxycortisol (cortodoxone, cortexolone)
Cortifen (cortiphen, kortifen)
Cortodoxone acetate
11β-Hydroxyprogesterone
16α,18-Dihydroxy-11-deoxycorticosterone
17α-Hydroxyaldosterone
18-Hydroxy-11-deoxycorticosterone
19-Norprogesterone
Aldosterone
Corticosterone
Corticosterone acetate
Corticosterone benzoate
Cortisol (hydrocortisone)
Benzodrocortisone (hydrocortisone benzoate)
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Cortisone
Cortisone acetate
Fludrocortisone (fludrocortone)
Fludrocortisone acetate
Mometasone
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Prednazoline
Prednicarbate (prednisolone ethylcarbonate propionate)
Prednimustine
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Prednisolone esters
Prednisone
Prednisone esters
Antagonists
Steroidal: 6β-Hydroxy-7α-thiomethylspironolactone
7α-Acetylthio-17α-hydroxyprogesterone
7α-Thiomethylspironolactone (SC-26519)
7α-Thioprogesterone (SC-8365)
7α-Thiospironolactone (SC-24813)
16α-Hydroxyprogesterone
17α-Hydroxyprogesterone (hydroxyprogesterone)
18-Deoxyaldosterone
18,19-Dinorprogesterone
Canrenoate potassium (potassium canrenoate)
Canrenoic acid (canrenoate)
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Dicirenone
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Metribolone
Mexrenoate potassium
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Mexrenone
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Oxprenoate potassium (RU-28318)
Pregnenolone
Progesterone
Prorenoate potassium
Prorenoic acid (prorenoate)
Prorenone
RO-14-9012
RU-26752
SC-5233 (spirolactone)
SC-8109
SC-11927 (CS-1)
SC-19886
SC-27169
Spirorenone
Spironolactone
Spiroxasone
Tibolone
Trimegestone
ZK-91587
ZK-97894
Nonsteroidal: Amlodipine
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Benidipine
BR-4628
Esaxerenone
Felodipine
Finerenone
Nifedipine
Nimodipine
Nitrendipine
PF-03882845
SM-368229
See also
Receptor/signaling modulators
Mineralocorticoids and antimineralocorticoids
Glucocorticoid receptor modulators
List of corticosteroids
Authority control
NDL: 00560334
Retrieved from "https://en.wikipedia.org/w/index.php?title=Aldosterone&oldid=829445687"
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text:
Rules of basketball
From Wikipedia, the free encyclopedia
Jump to: navigation, search
The rules of basketball are the rules and regulations that govern the play, officiating, equipment and procedures of basketball. While many of the basic rules are uniform throughout the world, variations do exist. Most leagues or governing bodies in North America, the most important of which are the National Basketball Association and NCAA, formulate their own rules. In addition, the Technical Commission of the International Basketball Federation (FIBA) determines rules for international play; most leagues outside North America use the complete FIBA ruleset.
Contents
[hide]
1 Original rules
2 Players, substitutes, teams and teammates
3 Shot clock and time limits
4 Fouls, free throws and violations
5 Equipment
6 Officiating and procedures
7 International Rules of Basketball
8 References
9 Further reading
10 External links
Original rules
In January 15, 1892, James Naismith published his rules for the game of "Basket Ball" that he invented:[1] The original game played under these rules was quite different from the one played today as there was no dribbling, dunking, three-pointers, or shot clock, and goal tending was legal.
The ball may be thrown in any direction with one or both hands.
The ball may be batted in any direction with one or both hands.
A player cannot run with the ball. The player must throw it from the spot on which he catches it, allowance to be made for a man who catches the ball when running at a good speed if he tries to stop.
The ball must be held in or between the hands; the arms or body must not be used for holding it.
No shouldering, holding, striking, pushing, or tripping in any way of an opponent. The first infringement of this rule by any person shall count as a foul; the second shall disqualify him until the next basket is made or, if there was evident intent to injure the person, for the whole of the game. No substitution shall be allowed.
A foul is striking at the ball with the fist, violation of rules three and four and such described in rule five.
If either side makes three consecutive fouls, it shall count a goal for the opponents (consecutive means without the opponents in the mean time making a foul).
A goal shall be made when the ball is thrown or batted from the grounds into the basket and stays there (without falling), providing those defending the goal do not touch or disturb the goal. If the ball rests on the edges, and the opponent moves the basket, it shall count as a goal.
When the ball goes out of bounds, it shall be thrown into the field of play and played by the first person touching it. In case of dispute the umpire shall throw it straight into the field. The thrower-in is allowed five seconds. If he holds it longer, it shall go to the opponent. If any side persists in delaying the game, the umpire shall call a foul on that side.
The umpire shall be the judge of the men and shall note the fouls and notify the referee when three consecutive fouls have been made. He shall have power to disqualify people according to Rule 5.
The referee shall be judge of the ball and shall decide when the ball is in play, in bounds, to which side it belongs, and shall keep the time. He shall decide when a goal has been made and keep account of the baskets, with any other duties that are usually performed by a scorekeeper.
The time shall be two fifteen-minute halves, with five minutes rest between.
The side making the most points in that time is declared the winner.
The original rules of basketball are on display to the public at the University of Kansas.
Players, substitutes, teams and teammates
Naismith's original rules did not specify how many players were to be on the court. In 1900, five players became standard, and players that were substituted were not allowed to re-enter the game.[citation needed] Players were allowed to re-enter a game once from 1921, and twice from 1934; such restrictions on substitutions were abolished in 1945 when substitutions became unlimited. Coaching was originally prohibited during the game, but from 1949, coaches were allowed to address players during a time-out.
Originally a player was disqualified on his second foul. This limit became four fouls in 1911 and five fouls in 1945, still the case in most forms of basketball where the normal length of the game (before any overtime periods) is 40 minutes. When the normal length is 48 minutes (this is the case with the National Basketball Association in the United States) a player is accordingly disqualified on his sixth foul.
Shot clock and time limits
See also: Defensive three-second violation
The first time restriction on possession of the ball was introduced in 1933, where teams were required to advance the ball over the center line within ten seconds of gaining possession. This rule remained until 2000, when FIBA reduced the requirement to eight seconds, the NBA following suit in 2001. The NCAA retains the 10-second rule for men's play, and adopted this rule for women's play starting with the 2013–14 season.[2] U.S. high schools, whose rules are drafted by NFHS, also use the 10-second rule for both sexes.
In 1936 the three-second rule was introduced. This rule prohibits offensive players from remaining near their opponents' basket for longer than three seconds (the precise restricted area is also known as the lane or the key). A game central to this rule's introduction was that between the University of Kentucky and New York University. Kentucky coach Adolph Rupp did not take one of his referees with him, despite being warned of discrepancies in officiating between the Midwest and East by Notre Dame coach George Keogan, and the game became especially rough. Because of this game and others, 6'5" (1.96 m) Kentucky All-American center Leroy Edwards is generally recognized as the player responsible for the 3 second rule.
While the rule was originally adopted to reduce roughness in the area between big men, it is now considered to prevent tall offensive players from gaining an advantage by waiting close to the basket. When the NBA started to allow zone defense in 2001, a three-second rule for defensive players was also introduced.
The shot clock was first introduced by the NBA in 1954, to increase the speed of play. Teams were then required to attempt a shot within 24 seconds of gaining possession, and the shot clock would be reset when the ball touched the basket's rim or the backboard, or the opponents gained possession. FIBA adopted a 30-second shot clock two years later, resetting the clock when a shot was attempted. Women's basketball adopted a 30-second clock in 1971. The NCAA adopted a 45-second shot clock for men while continuing with the 30-second clock for women in 1985. The men's shot clock was then reduced to 35 seconds in 1993, and further reduced to 30 seconds in 2015. FIBA reduced the shot clock to 24 seconds in 2000, and changed the clock's resetting to when the ball touched the rim of the basket. Originally, a missed shot where the shot clock expired while the ball is in the air constituted a violation. In 2003 the rule was changed so that the ball remains live in this situation, as long as it touched the rim. If the ball touches the rim and slightly bounces over the basketball hoop it will be called as a loose ball.
Fouls, free throws and violations
Dribbling was not part of the original game, but was introduced in 1901. At the time, a player could only bounce the ball once, and could not shoot after he had dribbled. The definition of dribbling became the "continuous passage of the ball" in 1909, allowing more than one bounce, and a player who had dribbled was then allowed to shoot.
Running with the ball ceased to be considered a foul in 1922, and became a violation, meaning that the only penalty was loss of possession. Striking the ball with the fist has also become a violation. From 1931, if a closely guarded player withheld the ball from play for five seconds, play was stopped and resumed with a jump ball; such a situation has since become a violation by the ball-carrier. Goaltending became a violation in 1944, and offensive goaltending in 1958.
Free throws were introduced shortly after basketball was invented. In 1895, the free throw line was officially placed fifteen feet (4.6 m) from the backboard, prior to which most gymnasiums placed one twenty feet (6.1 m) from the backboard. From 1924, players that received a foul were required to shoot their own free throws. One free throw shot is awarded to a player who was fouled while making a successful field goal attempt. If the field goal attempt is unsuccessful, two free throw shots are awarded (three if the player was attempting a three-point field goal). If an offensive player is fouled while not in the act of shooting, or if a player is fouled in a loose-ball situation, the penalty varies by level of play and the number of fouls accumulated by the opposing team in a given period.
In NCAA men's and all NFHS play:
If the player's team has 6 or fewer team fouls in the half, the team fouled gets possession of the ball.
If the team has 7 to 9 team fouls, the player fouled goes to the line for what is called "one-and-one" or the "bonus"—that is, if the player makes the first free throw, he gets the opportunity to attempt a second, but if he misses, the ball is live.
If the team has 10 or more fouls in the half, the player fouled gets two free throws, often called the "double bonus".
All overtime periods are considered an extension of the second half for purposes of accumulated fouls. Also, NFHS rules accumulate fouls per half, even though games are played in quarters.
In NCAA women's play (as of 2015–16, when the game changed from 20-minute halves to 10-minute quarters):
If the player's team has 4 or fewer team fouls in the quarter, the team fouled gets possession of the ball.
If the team has 5 or more fouls in the quarter, the player fouled gets two free throws—the "one-and-one" has now been removed from the women's game.
All overtime periods are considered an extension of the fourth quarter for purposes of accumulated fouls.
In the NBA:
If the player's team has 4 or fewer team fouls in the quarter, the team fouled gets possession of the ball.
Starting with the team's fifth foul in the quarter, the player fouled gets two free throws.
Overtime is not considered an extension of any quarter. Instead, the "penalty" of two free throws is triggered on the team's fourth foul in that overtime period (instead of the fifth).
Foul limits are reset in the last two minutes of a quarter or overtime period. If a team has not reached its limit of accumulated fouls, the first team foul in the last two minutes results in possession by the team fouled, and all subsequent fouls result in two free throws.
In the WNBA:
All foul limits are identical to those in the NBA, except that the team foul limit does not reset until the final minute of a quarter or overtime period.
In FIBA (full-court) play:
If the player's team has 4 or fewer team fouls in the quarter, the team fouled gets possession of the ball.
Starting with the team's fifth foul in the quarter, the player fouled gets two free throws.
During an interval of play, all team members entitled to play are considered as players.
The ball become dead when an official blows his whistle while the ball is live.
All overtime periods are considered an extension of the fourth quarter for purposes of accumulated fouls.
In FIBA 3x3 (half-court) play:
A player who is fouled on an unsuccessful field goal attempt receives one free throw if the attempt was from inside the 'three-point" arc, and two free throws if the attempt was from outside the arc. This reflects the different scoring of that variation, in which baskets from inside the arc are worth 1 point and those from outside the arc are worth 2 points.
If the player's team has 6 or fewer team fouls in the game, and the foul was not in the act of shooting, the team fouled gets possession of the ball.
Starting with the team's seventh foul in the game, the player fouled gets two free throws.
Starting with the team's 10th foul in the game, the player fouled gets two free throws, and the shooter's team gets possession of the ball.
A player has 10 seconds to attempt a free throw. If the player does not attempt a free throw within 10 seconds of receiving the ball, the free throw attempt is lost, and a free throw violation is called. A free throw violation also occurs if a free throw misses the backboard, rim, and basket. If a free throw violation is assessed on the last free throw awarded to a player in a given situation, possession automatically reverts to the opposing team.
A charge is physical contact between an offensive player and a defensive player. In order to draw an offensive charge the defensive player must establish legal guarding positioning in the path of the offensive player. If contact is made, the officials would issue an offensive charge. No points will be allowed and the ball is turned over. The defensive player may not draw an offensive charge in the "restricted zone" (see below for more details).[3]
Blocking is physical contact between the offensive player and the defensive player. Blocking fouls are issued when a defensive player interferes with the path of the offensive player in the shooting motion. Blocking fouls are easily called when the defensive player is standing in the "restricted zone".[3]
Restricted zone: In 1997, the NBA introduced an arc of a 4-foot (1.22 m) radius around the basket, in which an offensive foul for charging could not be assessed. This was to prevent defensive players from attempting to draw an offensive foul on their opponents by standing underneath the basket. FIBA adopted this arc with a 1.25 m (4 ft 1.2 in) radius in 2010.[4]
Equipment
The ball was to be an "ordinary Association football". In other words, a soccer ball.[5] The goal is placed 10 feet (3.05m) above the court. Originally a basket was used (thus "basket-ball"), so the ball had to be retrieved after each made shot. Today a hoop with an open-bottom hanging net is used instead.
Officiating and procedures
Main article: Official (basketball)
Originally, there was one umpire to judge fouls and one referee to judge the ball; the tradition of calling one official the "referee" and the other one or two the "umpires" has remained (the NBA, however, uses different terminology, referring to the lead official as "crew chief" and the others as "referees"). Today, both classes of officials have equal rights to control all aspects of the game. The NBA added a third official in 1988, and FIBA did so afterward, using it for the first time in international competition in 2006. The use of video evidence to inform referee's decisions has always been banned, except in the case of determining whether or not the last shot of a period was attempted before time expired. This exception was introduced by the NBA in 2002 and adopted by FIBA in 2006. The NCAA, however, has permitted instant replay for timing, the value of a field goal (two or three points), shot clock violations, and for purposes of disqualifying players because of unsportsmanlike conduct. The NBA changed its rules starting in 2007 to allow officials the ability to view instant replay with plays involving flagrant fouls, similar to the NCAA. In Italy's Serie A, an American football-style coach's challenge is permitted to challenge (at the next dead ball) an official's call on any situation similar to the NCAA.
The center jump ball that was used to restart a game after every successful field goal was eliminated in 1938, in favor of the ball being given to the non-scoring team from behind the end line where the goal was scored, in order to make play more continuous. The jump ball was still used to start the game and every period, and to restart the game after a held ball. However, the NBA stopped using the jump ball to start the second through fourth quarters in 1975, instead using a quarter-possession system where the loser of the jump ball takes the ball from the other end to start the second and third periods, while the winner of that jump ball takes the ball to start the fourth period from the other end of the court.
In 1981, the NCAA adopted the alternating possession system for all jump ball situations except the beginning of the game, and in 2003, FIBA adopted a similar rule, except for the start of the third period and overtime. In 2004, the rule was changed in FIBA that the arrow applies for all situations after the opening tap.
In 1976, the NBA introduced a rule to allow teams to advance the ball to the center line following any legal time-out in the final two minutes of the game. FIBA followed suit in 2006.
International Rules of Basketball
The most recent international rules of basketball were approved February 2, 2014 by FIBA and became effective October 1 of that year.[6]
There are eight rules encompassing 50 articles, covering equipment and facilities, regulations regarding teams, players, captains and coaches, playing regulations, violations, fouls and their penalties, special situations, and the officials and table officials. The rules also cover officials' signals, the scoresheet, protest procedure, classification of teams and television timeouts.
References
Jump up ^ "Naismith's Original 13 Rules". Retrieved October 2, 2017.
Jump up ^ Williamson, Debbie (August 2013). 2013-14 and 2014-15 Women's Basketball Rules. Indianapolis: The National Collegiate Athletic Association. p. 6.
^ Jump up to: a b NBA.com BLOCK-CHARGE. National Basketball Association.
Jump up ^ "The FIBA Central Board approves historic rule changes" (Press release). FIBA. April 26, 2008. Retrieved April 27, 2008.
Jump up ^ University of Kansas grad David Booth scores original basketball rules for $4.3M at memorabilia sale
Jump up ^ "Official Basketball Rules 2014" (pdf). International Basketball Federation. 2014. Retrieved October 27, 2014.
Further reading
Naismith, James (1941). Basketball: its origin and development. University of Nebraska Press. ISBN 0-8032-8370-9
External links
Rules of the Game @ usabasketball.com FIBA, NBA, and NCAA rules compared side-by-side.
Official Basketball rules @ fiba.com
"Official NBA rules - NBA rules and regulations" at nba.com
"NCAA Basketball Rulebook"
"Referee Signal – Picture Description of referee signal" at youth-basketball-tips.com
"FIBA / USA basketball rule differences and rule changes for various rule making bodies"
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