Pharmacology of the renal circulation

The circulatory response of the kidney to drugs is conditioned by a variety of factors, such as basal vascular tone, dietary sodium and structural changes in the renal vasculature which accompany aging and disease. In addition, any drug which affects systemic arterial pressure will activate renal autoregulatory processes, which are superimposed upon the direct effects of the drug on the renal circulation. Renal autoregulation in addition to passive pressure effects probably accounts for the relative constancy of renal blood flow during the administration of renal vasodilators such as nitroprusside, diazoxide and minoxidil. Renal vasodilators which have minor effects on systemic arterial pressure, such as dopamine and glucagon, increase renal blood flow. These effects have been employed clinically in low cardiac output states. A variety of drugs affect the renal circulation by modifying the effects of endogenous vasoactive substances. The mechanisms of action include: receptor blockade; ex, adrenergic and Ag II-mediated vasoconstriction: enhanced production by the administration of biochemical precursors; ex, arachidonic acid and I-dopa: inhibition of endogenous production; ex, prostaglandin synthetase inhibitors: and inhibition of breakdown of endogenous substances; ex, converting enzyme inhibition. The effect of each of these interventions will depend in part upon the rate of endogenous production of the relevant vasoactive material. The administration of diuretics affects renal blood flow in individually distinctive ways, the mechanisms of which have been only partially elucidated.