Renovascular resistance and noradrenaline

Abstract

Stimulation of the renal nerves can cause cortical vasoconstriction either by direct activation of vascular smooth muscle or by the generation of angiotensin II following renin release from the juxtaglomerular cells. High doses ( greater than 5 mug/min) of the renal neurotransmitter noradrenaline (NA) infused into the renal artery of the baboon causes cortical vasoconstriction. This NA-induced vasoconstriction is significantly reduced (P less than 0.001) by SQ20881, an inhibitor of converting enzyme, and by saralasin, a competitive inhibitor of angiotensin II. These results suggest that NA stimulates the renin-angiotensin mechanism. The further addition of the alpha-adrenergic blocking agent, phenoxybenzamine, to the NA-SQ20881 or NA-saralasin infusate completely abolishes NA-induced cortical vasoconstriction. These results suggest that NA-induced cortical vasoconstriction in the kidney is mediated by activation of both the renin-angiotensin system and alpha-adrenergic receptors.