Influence of Angiotensin Converting Enzyme Inhibition with Captopril on Blood Pressure and Adrenergic Function in Normal and Sodium Restricted Rats

Abstract

Observations with both captopril and teprotide suggest interplay of the renin angiotensin and sympathetic nervous systems during sodium depletion. We therefore examined adrenergic responses in normal or sodium restricted (8 days low sodium chow; trichlormethiazide 3 mg/kg, p.o., days 5–7) normotensive rats orally pretreated with placebo or captopril (3 or 10 mg/kg; twice on day 7, once on day 8) and pithed 2 hrs after the last dose. Consistent hypotension in conscious intact animals was observed only in sodium-depleted groups receiving captopril. Pressor responses to low frequency (2.5 Hz – 5 sec) sympathetic stimulation and phenylephrine were reduced in normal sodium, pithed normotensive Spraque-Dawley rats receiving 10, but not 3 mg/kg captopril and low sodium animals receiving both doses. Suppression of phenylephrine by captopril was accentuated in sodium-depleted groups. Pressor responses to angiotensin II were less in all salt-depleted animals receiving either placebo or captopril. Captopril failed to reduce tachycardia to either sympathetic nerve stimulation or isoproterenol. These effects of captopril suggest that angiotensin plays a role in maintenance of vascular, but not cardiac adrenergic function. This role is manifested at a post-junctional site and becomes critical in the sodium deficient state.