Motility and tone: α2 and β2 receptors have opposite effects. α2 receptors decrease motility and tone, while β2 receptors increase them. Sphincters are usually contracted by α receptors and relaxed by β receptors. Secretion is usually inhibited by α receptors and stimulated by β receptors. The gallbladder and ducts are relaxed by α receptors and contracted by β receptors.

Motility and tone: α receptors usually increase motility and tone, while the effect of β receptors is uncertain. The uterus is contracted by α receptors during pregnancy and relaxed by β receptors when not pregnant. Male sex organs are stimulated by α receptors, resulting in ejaculation and erection. Generalized secretion is increased by α and β receptors. The spleen capsule is contracted by α and β receptors, but relaxation is also observed.

Adrenal medulla: No known functional innervation.

Liver: α and β receptors stimulate glycogenolysis and gluconeogenesis. β receptors also increase secretion.

Fat cells: α and β1 receptors stimulate lipolysis.

Dilation predominates in situ due to metabolic autoregulatory phenomena. Cholinergic vasodilation at these sites is of questionable physiological significance. Over the usual concentration range of physiologically released circulating epinephrine, a β receptor response (vasodilation) predominates in blood vessels of skeletal muscle and the liver, while an α receptor response (vasoconstriction) predominates in blood vessels of other abdominal viscera. The renal and mesenteric vessels also contain specific dopaminergic receptors, which cause dilation, but their physiological significance has not been established. The sympathetic cholinergic system causes vasodilation in skeletal muscle, but this is not involved in most physiological responses.

The adrenergic fiber terminates at inhibitory β receptors on smooth muscle fibers and inhibitory α receptors on parasympathetic cholinergic (excitatory) ganglion cells of the Auerbach plexus.

The effect of β receptor activity is regulated in multiple ways. α1 receptors can antagonize β receptor activity. Prolonged exposure to agonists can desensitize β receptors through phosphorylation. The number of β receptors can also be regulated. They can be internalized, resulting in decreased receptor numbers, or upregulated in certain circumstances such as after denervation. Note that the number of α receptors is also regulated.

In addition to norepinephrine, sympathetic postganglionic neurons release neuropeptides such as somatostatin and neuropeptide Y. For example, cells that release both norepinephrine and somatostatin innervate the mucosa of the gastrointestinal tract, while cells that release both norepinephrine and neuropeptide Y innervate blood vessels in the gut and the limb. Another chemical mediator in sympathetic postganglionic neurons is adenosine triphosphate (ATP).
Motilityandtoneα2,β2Decrease + Increase+++ Sphinctersα Contraction(usually)+ Relaxation(usually)+ SecretionInhibition(?)Stimulation+++ Gallbladder and Ducts Relaxation+ Contraction+
Motilityandtoneα Increase(usually)Increase(?)Uterus α,β2Pregnant:contraction(α);Variable nonpregnant:relaxation(β)Sex Organs, Male α Ejaculation+++ Erection+++ + Generalizedsecretion+++ Spleen Capsule α,β2Contraction+++;relaxation+ —
Adrenal Medulla —SecretionofepinephrineandnorepinephrineLiver α,β2Glycogenolysis,gluconeogenesis β2Increasedsecretion+ —Fatcellsα,β1Lipolysis
FromGoodmanLS,GilmanA.The Pharmacological Basis of Therapeutics. 6thed.NewYork:Macmillan;1980.aAlongdash(—)signifiesnoknownfunctionalinnervation.bResponsesaredesignated+ to+++ toprovideanapproximateindicationoftheimportanceofadrenergicandcholinergicnerveactivityincontrolofthevariousorgansandfunctionslisted.cDilationpredominatesinsitubecauseofmetabolicautoregulatoryphenomena.dCholinergicvasodilationatthesesitesisofquestionablephysiologicalsignificance.eOvertheusualconcentrationrangeofphysiologicallyreleasedcirculatingepinephrine,aβ receptorresponse(vasodilation)predominatesinbloodvesselsofskeletalmuscleandtheliver,andanα receptorresponse(vasoconstriction)predominatesinbloodvesselsofotherabdominalviscera.Therenalandmesentericvesselsalsocontainspecificdopaminergicreceptors,activationofwhichcausesdilation,buttheirphysiologicalsignificancehasnotbeenestablished.fThesympatheticcholinergicsystemcausesvasodilationinskeletalmuscle,butthisisnotinvolvedinmostphysiologicalresponses.gIthasbeenproposedthatadrenergicfibersterminateatinhibitoryβ receptorsonsmoothmusclefibersandatinhibitoryα receptorsonparasympatheticcholinergic(excitatory)ganglioncellsoftheAuerbachplexus.hDependsonthestageofthemenstrualcycle,theamountofcirculatingestrogenandprogesterone,andotherfactors.iPalmsofthehandsandsomeothersites(“adrenergicsweating”).jThereissignificantvariationamongspeciesinthetypeofreceptorthatmediatescertainmetabolicresponses.
β receptor activity is controlled in a number of ways. It can be antagonized by the action of α1 receptors. The β receptors can also be desensitized by phosphorylation with prolonged exposure to agonists. Regulation of β receptor numbers represents a third control mechanism. For example, β receptor numbers can be decreased by being internalized. Alternatively, β receptor numbers can be increased (upregulated) in certain circumstances: for example, after denervation. Note that the number of α receptors is likewise regulated.
In addition to releasing norepinephrine, sympathetic postganglionic neurons release neuropeptides such as somatostatin and neuropeptide Y. For example, cells that release both norepinephrine and somatostatin supply the mucosa of the gastrointestinal tract, and cells that release both norepinephrine and neuropeptide Y innervate blood vessels in the gut and the limb. Another chemical mediator in sympathetic postganglionic neurons is adenosine triphosphate (ATP).