The effect of angiotensin II on the pressor response of the mesenteric vascular bed to periarterial adrenergic nerve stimulation (PNS) was compared between spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY). Angiotensin II (1-20 ng/ml) caused a marked potentiation of the vasoconstrictor response to PNS (8 Hz, 2 msec, for 30 sec) in a concentration-dependent manner without significantly affecting the base-line perfusion pressure in either WKY or SHR. The facilitatory effect of angiotensin II was significantly greater in SHR than in WKY preparations. The effective concentration for the peptide in SHR was approximately one-third of that found in WKY. Angiotensin II also potentiated the pressor response to exogenously administered norepinephrine (NE, 50 ng) in both WKY and SHR. The degree of potentiation of the response to PNS was greater than that to NE in SHR, while this differential was found only at high concentrations of angiotensin II on the WKY. The facilitatory effect of angiotensin II on the pressor response to either PNS or NE was markedly reduced by [Sar1-Ile8]angiotensin II (200 ng/ml) in both WKY and SHR. Angiotensin II caused further potentiation of the vasoconstrictor response to PNS or NE infusion in the presence of cocaine (5 micrograms/ml), which was of a greater magnitude in SHR than in WKY. These results suggest that the presynaptic facilitatory modulation of adrenergic vascular neurotransmission, mediated by angiotensin II receptors, is enhanced in the perfused mesenteric vascular bed of SHR.