adrenergic receptor

(redirected from Adrenoreceptors)

adrenergic receptor

Etymology: L, ad + ren, kidney; Gk, ergon, work; L, recipere, to receive
a site in a sympathetic effector cell that reacts to adrenergic stimulation. Two types of adrenergic receptors are recognized: alpha-adrenergic, which act in response to sympathomimetic stimuli, and beta-adrenergic, which block sympathomimetic activity. In general, stimulation of alpha receptors is excitatory of the function of the host organ or tissue, and stimulation of the beta receptors is inhibitory.

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.

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

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.
References in periodicals archive ?
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.
Background: Clonidine activates peripheral [alpha]-2 adrenoreceptors and influences glycemic levels.
Dexmedetomidine, acts via a2 adrenoreceptors and also provides analgesia, sedation and anxiolysis.
This can be explained on the basis of alpha 2 agonist produce sedation by central action by inhibition of substance P release in the nociceptive pathway at the level of dorsal root neuron and by activation of alpha 2 adrenoreceptors in locus coeruleus.
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.
Endothelial [beta]3- adrenoreceptors mediate nitric oxide-dependent vasorelaxation of coronary microvessels in response to the third-generation [beta]-blocker nebivolol," Circulation, vol.
Many plants, which have a stimulatory effect on the CNS, synthesize substances that contain phenylethylamine or xanthine structures that are able to enhance catecholaminergic effects and/or to act on adrenoreceptors [3].
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.
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.