Atrial receptor

D. Sarsero, P. Molenaar, A.J. Kaumann, N.S. Freestone, Putative /t4-adrenoceptors in rat ventricle mediate increases in contractile force and cell Ca2-i- Comparison with atrial receptors and relationship to (-)-[3H]-CGP 12177 binding, Br. J. Pharmacol. 128(1999) 1445-1460. 

Receptors linked to guanylyl cyclase and which catalyze the formation of guanosine triphosphate (GMP) to guanosine-3A -cychc monophosphate (cychc GMP) include those for atrial natriuretic factor (ANF) and endothehal-derived relaxing factor (EDRF), mediating vasodilatation, and nitric oxide [10102 3-9], NO, or a clearly related derivative. 

FIGURE 2.17 Differential efficiency of receptor coupling for cardiac function, (a) Guinea pig left atrial force of contraction (inotropy, open circles) and rate of relaxation (lusitropy, filled circles) as a function (ordinates) of elevated intracellular cyclic AMP concentration (abscissae). Redrawn from [6]. 

Adenosine activates the atrial Ai-adenosine receptor, which opens the Ik Ado channel leading to... 

Urodilatin is a peptide similar to atrial natriuretic peptide, which is produced in the distal tubule of the kidney and promotes sodium excretion and diuresis by acting on receptors localized on the luminal site of the collecting duct of the nephron. 

A G-protein-mediated effect has an absolute requirement for GTP. Reference has already been made to the requirement for GTP in reconstituting hormone-stimulated adenylate cyclase activity. A similar requirement can be demonstrated when the effector is an ion channel, such as the cardiac atrial inward-rectifier K+ channel which is activated following stimulation of the M2 muscarinic acetylcholine receptor. Thus, in the experiment illustrated in Figure 7.8, the channel recorded with a cell-... 

Effects mediated by G-protein coupled receptors (GPCRs) are very much slower than those mediated by, for example, ligand-gated ion channels, primarily because more steps are involved between activation of the receptor and the final response. For example, even in a simple, three-step, G-protein-mediated effect, such as the opening of atrial GIRK channels following the activation of M2 muscarinic receptors by acetylcholine, which follows the scheme ... 

The vascular endothelium produces a number of substances that are released basally into the blood vessel wall to alter vascular smooth muscle tone. One such substance is endothelin (ET-1). Endothelin exerts its effects throughout the body, causing vasoconstriction as well as positive inotropic and chronotropic effects on the heart. The resulting increases in TPR and CO contribute to an increase in MAP. Synthesis of endothelin appears to be enhanced by many stimuli, including Ag II, vasopressin, and the mechanical stress of blood flow on the endothelium. Synthesis is inhibited by vasodilator substances such as prostacyclin, nitric oxide, and atrial natriuretic peptide. There is evidence that endothelin is involved with the pathophysiology of many cardiovascular diseases, including hypertension, heart failure, and myocardial infarction. Endothelin receptor antagonists are currently available for research use only. 

A more moderate stimulus for thirst and ADH secretion is a decrease in extracellular fluid, or plasma volume. This stimulus involves low-pressure receptors in the atria of the heart as well as baroreceptors in the large arteries. A decrease in plasma volume leads to a decrease in atrial filling, which is detected by low-pressure receptors, and a decrease in MAP, which the baroreceptors detect. Each of these receptors then provides excitatory inputs to the thirst center and to the ADH-secreting cells. 

Vandelen, R.L., Arcuri, K.E., and Napier, M.A. (1985) Identification of a receptor for atrial natriuretic factor in rabbit aorta membranes by affinity cross-linking./. Biol. Chem. 260, 10889-10892. 

There are seven membrane forms of GC, designated GC-A to GC-G [33], Two forms, GC-A and GC-B (Mr = 120kDa), serve as receptors for atrial natriuretic peptide (ANP) and related peptides. ANP is a 28-amino-acid peptide isolated originally from cardiac atria as an important factor in the regulation of sodium excretion and blood pressure. GC-A binds ANP, as well as brain natriuretic peptide (BNP), and is located in vascular tissue and kidney. 

Gordienko D V, Bolton TB, Cannell MB 1998 Variability in spontaneous subcellular Ca2+ release in guinea-pig ileum smooth muscle cells. J Physiol 507 707-720 Ho R, Shao Z 1991 Axial resolution of confocal microscopes revisited. Optiik 88 147—154 Holz GG, Leech CA, Heller RS, Castonguay N, Habener JF 1999 cAMP-dependent mobilization of intracellular Ca2+ stores by activation of ryanodine receptors in pancreatic [j cells. A Ca2+ signaling system stimulated by the insulinotropic hormone glucagon-like peptide-1-(7-37). J Biol Chem 274 14147-14156 Lipsius SL, Hiiser J, Blatter LA 2001 Intracellular Ca2+ release sparks atrial pacemaker activity. News Physiol Sci 16 101-106... 

Jones, S.B. and King, L.B. 1995, Muscarinic cholinergic receptors in brain and atrial membranes of adult Brook Trout Salvelinus fontinalis measured by radiolignad binding techniques. Comp. Biochem. Physiol. 112 43-50. 

Atrial natriuretic peptide binds to the GPCR receptor. 

Atrial natriuretic factor (ANF), produced by cells in the atrium of the heart in response to distension, binds the ANF receptor in vascular smooth muscle and in the kidney. The ANF receptor spans the membrane and has guanylate cyclase activity associated wMi the cytoplasmic domain. It causes relaxation of vascular smooth muscle, resulting in vasodilation, and in the kidney it promotes sodium and water excretion. 

Naturally occurring peptides can be altered in size and structure, and randomization of residues can be introdnced into libraries for the identification of peptides with improved characteristics or improved binding specificity. Snch an approach has been used to select re-ceptor-spedfic variants of atrial natrinretic peptide (ANP) with improved expression in E. coli and spedficity for jnst one form of the ANP receptors [29]. 

This group consists of j3-adrenergic receptor blockers, the antiarrhythmic activity of which is associated with inhibition of adrenergic innervation action of the circulatory adrenaline on the heart. Because all 8-adrenoblockers reduce stimulatory sympathetic nerve impulses of catecholamines on the heart, reduce transmembrane sodium ion transport, and reduce the speed of conduction of excitation, sinoatrial node and contractibility of the myocardium is reduced, and automatism of sinus nodes is suppressed and atrial and ventricular tachyarrhythmia is inhibited. 

Amiodarone s antiarrhythmic action is connected to its ability to block K, Na, and Ca channels while noncompetitively blocking a- and j3-adrenergic receptors of the heart, thus prolonging the action potential and effective refractive period of atrial cells, atrioventricular junctions, and ventricles of the heart, which is accompanied by decreased automatism of sinus node and slowing of atrioventricular conductivity. 

H3-receptors have been identified in the central nervous system. They are located on presynaptic membranes and serve as inhibitory autoreceptors at histaminergic neurons. They are also found on certain human autonomic nerve endings and in atrial tissue where they may inhibit norepinephrine release during ischemia. 

---