Blockade by saralasin of adrenergic potentiation induced by renin-angiotensin system

Participation of the renin-angiotensin system in the potentiation of responses to adrenergic nerve stimulation in the pump-perfused dog paw was studied during suprarenal aortic constriction. Vasoconstrictor responses in the paw were elicited by norepinephrine injected intra-arterially and by sympathetic nerve stimulation in a control session and during suprarenal aortic constriction (cephalad to the origin of one or two renal arteries). Aortic constriction decreased renal blood flow by approximately 50% and increased systemic blood pressure and plasma renin activity. The vasoconstrictor responses to norepinephrine and nerve stimulation were not significantly affected when the constriction was cephalad to only one renal artery, but there was a 31% increase in the response to stimulation at 5 Hz during aortic constriction above two renal arteries. There was an approximate 2-fold greater increase in plasma renin activity during the latter than in the former case. Saralasin administered intra-arterially to the paw reversed the adrenergic potentiating effect of aortic constriction. These results indicate that when the renin-angiotensin system is activated by restricting renal blood flow, sufficient circulating endogenous angiotensin is formed to cause a moderate adrenergic potentiating effect in the canine cutaneous circulation of the paw.