Autonomics: GPCRs Flashcards
α1 receptor
sympathetic, Gq
↑ vascular smooth muscle contraction, ↑ pupillary dilator muscle contraction
(mydriasis), ↑ intestinal and bladder sphincter muscle contraction
α2 receptor
sympathetic, Gi
↓ sympathetic (adrenergic) outflow, ↓ insulin release, ↓ lipolysis, ↑ platelet
aggregation, ↓ aqueous humor production
β1 receptor
sympathetic, Gs
↑ heart rate, ↑ contractility (one heart), ↑ renin release, ↑ lipolysis
β2 receptor
sympathetic, Gs
Vasodilation, bronchodilation (two lungs), ↑ lipolysis, ↑ insulin release,
↑ glycogenolysis, ↓ uterine tone (tocolysis), ↑ aqueous humor production,
↑ cellular K+ uptake
β3 receptor
sympathetic, Gs
↑ lipolysis, ↑ thermogenesis in skeletal muscle, ↑ bladder relaxation
M1 receptor
parasympathetic, Gq
Mediates higher cognitive functions, stimulates enteric nervous system
M2 receptor
parasympathetic, Gi
↓ heart rate and contractility of atria
M3 receptor
parasympathetic, Gq
↑ exocrine gland secretions (eg, lacrimal, sweat, salivary, gastric acid),
↑ gut peristalsis, ↑ bladder contraction, bronchoconstriction, ↑ pupillary
sphincter muscle contraction (miosis), ciliary muscle contraction
(accommodation), ↑ insulin release, endothelium-mediated vasodilation
D1 receptor
dopamine, Gs
Relaxes renal vascular smooth muscle, activates direct pathway of striatum
D2 receptor
dopamine, Gi
Modulates transmitter release, especially in brain, inhibits indirect
pathway of striatum
H1 receptor
histamine, Gq
↑ nasal and bronchial mucus production, ↑ vascular permeability,
bronchoconstriction, pruritus, pain
H2 receptor
histamine, Gs
↑ gastric acid secretion
V1 receptor
vasopressin, Gq
↑ vascular smooth muscle contraction
V2 receptor
vasopressin, Gs
↑H2O permeability and reabsorption via upregulating aquaporin-2 in collecting twobules (tubules) of kidney, ↑ release of vWF
autonomic drugs
Release of norepinephrine from a sympathetic nerve ending is modulated by NE itself, acting on
presynaptic
α2-autoreceptors –> negative feedback.
Amphetamines use the NE transporter (NET) to enter the presynaptic terminal, where they utilize
the vesicular monoamine transporter (VMAT) to enter neurosecretory vesicles. This displaces NE
from the vesicles. Once NE reaches a concentration threshold within the presynaptic terminal,
the action of NET is reversed, and NE is expelled into the synaptic cleft, contributing to the
characteristics and effects of ↑ NE observed in patients taking amphetamines.
