Renovascular resistance and noradrenaline

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 (> 5 μg/min) of the renal neurotransmitter noradrenaline (NA) infused into the renal artery of the baboon causes cortical vasconstriction. This NA induced vasoconstriction is significantly reduced (P < 0.001) by SQ 20881, an inhibitor of converting enzyme, 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 drenergic blocking agent, phenoxybenzamine, to the NA SQ 20881 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 α adrenergic receptors.