Intrarenal vasodilator systems: NO, prostaglandins and bradykinin. An integrative approach.

Intrarenal microcirculation is under hormonal, paracrine and neural control. Of particular interest is circulation in the renal medulla: its perfusion seems critical for long term control of arterial pressure. Exposure of the organism to adverse conditions often leads to activation of vasopressor factors, such as renin/angiotensin, renal sympathetic input or vasopressin; this helps maintain arterial pressure but endangers renal circulation. Fortunately, it is protected by intrarenal vasodilators: nitric oxide, prostaglandins, bradykinin and others. The potency of NO to oppose intrarenal vasoconstrictors may differ between individual factors: it is substantial in the case of renal sympathetic input whereas the constrictor influence of angiotensin II in the medulla seems to be offset mostly by intrarenal prostaglandins. Although these are commonly regarded as intrarenal vasodilators, our new data show that this is so only in the renal medulla. In the cortex they exert modest vasoconstriction, probably mediated by EP3 receptors. The role of bradykinin as intrarenal vasodilator is not yet known in sufficient detail, its effect is most pronounced in the inner medulla. The source of vasoactive kinins is uncertain, they could reach intrarenal microvasculature from the sites of synthesis in tubular cells but the synthesis in the vessels themselves cannot be excluded.