adrenergic receptor

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Adrenergic Receptor

Any of a family of G protein-coupled cell membrane receptors which receive neuronal impulses from postganglionic adrenergic fibres of the sympathetic nervous system, which are divided into:
(1) Alpha receptors, which evoke an excitatory response of smooth muscle cells to catecholamines. Alpha receptors are divided into alpha1 (Gq) and alpha2 (Gi) coupled receptors.
Selective agonist, alpha receptor Phenylephrine
Alpha receptor effects Vasoconstriction, reduced GI tract motility.
(2) Beta receptors, which dampen the response to catecholamines. Beta receptors are divided into beta1, beta2, beta3, which are linked to Gs, and adenylate cyclase, increasing cAMP, which in turn drives cAMP-dependent protein kinase that mediates intracellular events.
Selective agonist, beta receptor Isoprenaline
Beta receptor effects Increased cardiac output, increased renin secretion from juxtaglomerular cells, increased gastric ghrelin secretion, smooth muscle relaxation resulting in bronchodilation, reduced GI motility, relaxation of detrusor muscle of the bladder, lipolysis, glycogenolysis and gluconeogenesis, increased renin secretion, insulin secretion, vasodilation, anabolism and thermogenesis of skeletal muscle.
Segen's Medical Dictionary. © 2012 Farlex, Inc. All rights reserved.

adrenergic receptor

Neurophysiology Any of a family of cell membrane receptors that receive neuronal impulses from postganglionic adrenergic fibers from the sympathetic nervous sytem, which are divided into α receptors, which results in an excitatory response of smooth muscle cells to catecholamines, and β receptors, which result in an inhibitory response to catecholamines; the GI tract is an exception, in that either α or β receptor stimulation results in relaxation
McGraw-Hill Concise Dictionary of Modern Medicine. © 2002 by The McGraw-Hill Companies, Inc.

Adrenergic receptor

There are three families of adrenergic receptors, alpha1, alpha2 and beta, and each family contains three distinct subtypes. Each of the nine subtypes are coded by separate genes, and display specific drug specificities and regulatory properties.
Gale Encyclopedia of Medicine. Copyright 2008 The Gale Group, Inc. All rights reserved.
References in periodicals archive ?
The original method of RAS is yet to be completely explained, nevertheless it is said that activation of alpha adrenergic receptors present in the smooth muscles are involved in the process.6 These alpha adrenoreceptors are present abundantly in the radial arteries.
The pathogenic role of [beta]1-adrenoreceptor autoantibodies was confirmed in animal experiments in which peptides corresponding to the second extracellular loop of [beta]1 adrenoreceptors could trigger similar changes in the myocardium to those observed in dilated cardiomyopathy patients [146].
The sedative effect of dexmedetomidine is probably mediated by the activation of presynaptic a-2 adrenoreceptors in the locus coeruleus, leading to inhibition of release of norepinephrine, along with it, inhibition of adenylate cyclase may lead to hypnotic response.[22] Our study also showed that dexmedetomidine group had higher sedation scores which was supported by Salgado et al.
Dexmedetomidine, acts via a2 adrenoreceptors and also provides analgesia, sedation and anxiolysis.
The main action of the clonidine is the decreases in the level of peripheral norepinephrine release by stimulating the prejunctional inhibitory [alpha]-2 adrenoreceptors. It inhibits central neural transmission in the dorsal horn by presynaptic and postsynaptic mechanism and directly in spinal preganglionic sympathetic neurons.
Mirtazapine blocks the presynaptic [alpha]-2 adrenoreceptors in both the central and peripheral nervous systems, while its affinity to [alpha]-1 adrenoreceptors is less marked.
Ghisdal et al., "Endothelial [beta]3- adrenoreceptors mediate nitric oxide-dependent vasorelaxation of coronary microvessels in response to the third-generation [beta]-blocker nebivolol," Circulation, vol.
Beta blockers, particularly propranolol, are considered first-line therapy for drug-induced akathisia, with a dosage of 20 to 40 mg twice daily used to relieve symptoms (26) The effect can be explained by adrenergic terminals in the locus ceruleus and ending in the nucleus accumbens and prefrontal cortex stimulate [beta] adrenoreceptors. (5-27) Although multiple small studies and case reports (26-28-32) support the use of beta blockers to treat drug-induced akathisia, the quality of evidence of their efficacy is controversial.
Alpha-1A adrenoreceptors are a principal contributor in phenylephrine-induced ureteral contraction in the human isolated ureter.
[20] suggest that EC HSP 72 is released as a result of sympathetic nervous system activation, where norepinephrine binds to a 1 adrenoreceptors, causing an increase in intracellular calcium, thus stimulating the release exosomes containing HSP 72.
Dexmedetomidine produces analgesic effects by an action on [alpha]2 adrenoreceptors within the locus cerulus and the spinal cord.
The alpha-2 adrenoreceptors inhibit release of nor- adrenaline acetyl choline serotonin dopamine substance P and other neurotransmitters suppress neuronal excitability cause sedation anti-nociception hypotension and bradycardia (Aantaa et al.