G protein linked 2nd messengers Flashcards
sympathetic
A1 A2 B1 B2: QISS
A1: smooth muscle contraction, papillary dilator contration, increase intestinal and bladder sphincter contractio
A2: decrease sympathetic outflow, decrease insulin release, decrease lipolysis, increase platelet aggregation
B1: increase HR, increase contractility, increase RENIN release, increase lipolysis
B2: vasodilation, bronchodilation, increase HR, increase contractivity, increase lipolysis, increase insulin, decrease uterone tone, ciliary muscle relaxation, increase AQUEOUS humor production.
Parasym
M1 M2 M3 = QIQ (KICK)
M1: CNS, enteric nervous system
M2: decrease HR and contractility of atria
M3: increase exocrine gland secretion (lacrimal, gastric), increase gut peristalsis, increase bladder contraction, bronchoconstriction, increase pupillary sphincter constriction (miosis), ciliary muscle contraction (accomodation)
Dopamine
D1 D2 = SI (YES, pleasure)
D1: relaxes renal vascular smooth muscle
D2: modulates transmitter release, especially in brain
Histamine
H1 H2 = QS
H1: increase nasal bronchial mucus production, contraction of bronchioles, pruritus, and pain
H2: increase gastric acid secretion
Vasopression
V1 V2 = QS
V1: increase vascular smooth muscle contraction
V2: increase H2O permeability and reabsorption in the collecting tubule of the kidney
Gq
Gq => phospholipase C => PIP2 =>
DAG (activate protein kinase C) and
IP3 (increases Ca2+ -> smooth muscle contraction)
Gs, Gi
Gs activates and Gs inhibits
Adenylyl cyclase => ATP to cAMP => protein kinase A =>
Increase Ca2+ in heart
Blocks myosin light-chain kinase (smooth muscle)
Autonomic drugs: cholinergic
Hemicholinium: blocks choline reuptake
Vasamicol: blocks ChAT, transfering ACh into vesicles
Autonomic drugs: noradrenergic
Metyrosine: blocks from tyrosine to dopa
Reserpine: blocks transferring dopamine into vesicle
Guanethidine, bretylium: blocks NE release from vesicle
Amphetamine: induces NE release from vesicle
Cocaine, TCA, amphetamine: blocks reuptake from junction
Noradrenergic nerve terminal regulation
Release of NE from a sympathetic nerve ending is modulated by NE itself, acting on presynpatic A2 autoreceptors, and by ACh, angiotensin II, and other substances.