Abstract
Sympathetic nerves may modify various aspects of renal function including renal haemodynamics, renin secretion and sodium output. In a series of experiments we found that within the human kidney alpha 2-adrenoceptors are of greater importance than alpha 1-receptors in mediating the adrenergic effects. For instance, intrarenal infusion of an alpha 1-antagonist has a small effect on renal perfusion, whereas blockade of alpha 2-receptors increases renal flow profoundly. There is evidence that the relevant receptors are located at a postjunctional site. Alpha 2-receptors also play an inhibitory role in renin secretion. Recent data suggest that the alpha 2-receptor, which reduces renin release, is located presynaptically. Thus, stimulation of this receptor reduces noradrenaline overflow, and hence diminishes beta-adrenoceptor mediated increases in renin.
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