Effect of angiotensin III (des-Asp1-angiotensin II) on the vascular adrenergic neurotransmission in spontaneously hypertensive rats.

The effects of angiotensin III (des-Asp1-angiotensin II) on the pressor responses of the perfused mesenteric vascular bed to periarterial nerve stimulation (PNS) and exogenously administered noradrenaline (NA) of spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY) were compared. Angiotensin III (10, 20, 30 and 50 ng/ml) induced a marked potentiation of the pressor response to PNS (8 Hz) in a concentration-dependent manner with a slight elevation of the basal perfusion pressure in both SHR and WKY. The facilitatory effect of angiotensin III was blocked by [Sar1,Ile8]angiotensin II (200 ng/ml) and did not significantly differ for SHR and WKY. Angiotensin III also potentiated the pressor response to infusion of NA (50 ng) to the same extent in SHR and WKY. The degree of potentiation of the response to NA was similar to that to PNS in both WKY and SHR. Perfusion of angiotensin III (50 ng/ml) did not alter the increase in the 3H-efflux evoked by PNS (8 Hz) in the perfused mesenteric vascular bed prelabelled with [3H]NA, whereas the peptide potentiated significantly the pressor response to PNS in WKY and SHR to the same extent. These results suggest that angiotensin III postsynaptically facilitates the adrenergic neurotransmission of the mesenteric vascular bed to the same extent in WKY and SHR.