Chronic treatment of the spontaneously hypertensive rat with captopril attenuates responses to noradrenaline in vivo but not in vitro.

We have studied the attenuation by captopril of sympathetic neurotransmission in spontaneously hypertensive rats. Captopril (4 mg/kg for 15-17 days or 20 mg/kg for 4 days) was delivered i.v. by osmotic minipump. The higher dose lowered blood pressure, the lower dose did not. Both doses inhibited converting enzyme activity. In the pithed rat, both doses attenuated responses to exogenous noradrenaline and sympathetic nerve stimulation. In isolated tail arteries removed from captopril-treated rats, responses to sympathetic nerve stimulation and exogenous noradrenaline were the same as in controls. Perfusion of the tail artery of control rats with captopril, angiotensin I or angiotensin II had no effect on basal perfusion pressure or on vasoconstriction induced by exogenous noradrenaline or sympathetic nerve stimulation. Our results are consistent with the hypothesis that: 1. the attenuation of sympathetic neurotransmission by captopril depends upon the presence of an intact renin-angiotensin system, and 2. captopril has no direct postsynaptic effect in the isolated tail artery preparation.