Adrenergic receptor agonism

Inotropic activity is mediated through cardiac b -,-adrenergic receptors. In addition to an enhanced force of contraction (inotropy), stimulation of the b rreceptor also results in a variable degree of increase in sinus node firing rate (chronotropy), an increase in atrioventricular conduction velocity (dromotropy), and a decrease in the excitation threshold (bathmotropy).

Beta-2-receptors and a1-adrenergic receptors also exist in the myocardium and may mediate an important component of inotropic effect in the presence of chronic congestive heart failure and cardiomyopathy. Normally, about 80 per cent of inotropic action is mediated through the b rreceptor. However, in chronic congestive heart failure there is a persistent elevation of circulating catecholamines, culminating in downregulation of the cardiac b rreceptor. The relative proportion of b2-receptor-induced inotropic effect doubles from 20 to 40 per cent of total inotropic activity.

A small component of inotropic effect is mediated via the a1-adrenergic receptor, which also becomes more important in congestive heart failure and endstage cardiomyopathy. The a-receptor is coupled to phospholipase C on the inner layer of the sarcolemma by G q protein. Stimulation induces guanidosine triphosphate to cleave phosphatidyl inositol into inositol triphosphate, which releases calcium from the sarcoplasmic reticulum, and diacylglycerol, which activates protein kinase C and opens the calcium channel in the sarcolemma. The subsequent chain of events is similar to that of b-receptor activation. Importantly, however, the inotropic effect is independent of cAMP.

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