Angiotensin II-mediated renal vasoconstriction amenable to alpha 1-adrenoceptor blockade

Renal adrenergic interactions of intravenously and intrarenal arterially administered angiotensin II were studied in the anesthetized rabbit. Systemic arterial blood pressure and left renal blood flow were monitored. Bolus doses of angiotensin II, 50 and 100 ng/kg given intravenously, caused an immediate reduction in renal blood flow followed by a more sustained vasoconstrictor response. Prazosin, 5 micrograms/kg/min, infused intrarenal arterially, decreased both components of the reduced renal blood flow, suggesting adrenergic contribution to the response. Renal denervation reduced significantly the immediate response to angiotensin II without affecting the sustained response; administration of prazosin after denervation caused a further decrease in the response. Left adrenalectomy had no significant effect on the angiotensin II-induced renal blood flow response, ruling out the possible contribution of adrenal catecholamine release via the adrenal rete. In animals that had undergone renal denervation and left adrenalectomy, the renal blood flow response to intrarenal arterial injection of subpressor doses of angiotensin II (5 and 10 ng/kg) was reduced by the infusion of prazosin. It is concluded that angiotensin II-induced renal vasoconstriction is contributed to by adrenergic actions dependent in part on intact renal nerves, but also by a component not requiring an intact nerve supply.