Key result
Enalapril produces nonuniform end-organ responses to Ang I, suggesting intrarenal conversion to Ang II.
Why the study?
Does ACE inhibition with enalapril alter the pressor, renal vascular, and adrenal responses to Angiotensin I infusion in healthy men on a low-salt diet?
Does ACE inhibition with enalapril alter the pressor, renal vascular, and adrenal responses to Angiotensin I infusion in healthy men on a low-salt diet?
Answers are grounded in this paper and cite their sources.
ACE inhibition leads to nonuniform changes in the response to exogenous Angiotensin I, suggesting intrarenal conversion of Ang I to Ang II.
To examine the influence of angiotensin-converting enzyme (ACE) on pressor, renal vascular, and adrenal responses during angiotensin I (Ang I) infusion, we studied 10 normotensive, healthy men. Each was in balance with a 10-mEq sodium, 100-mEq potassium intake and was studied before and during ACE inhibition with enalapril. Ang I (3, 10, and 30 ng/kg/min) was infused in each subject. Then ACE inhibition was instituted with enalapril for 3 days, which induced the anticipated fall in blood pressure, plasma Ang II, and aldosterone concentration, and rise in renal plasma flow. During ACE inhibition only the 30-ng/kg/min Ang I dose raised plasma Ang II levels. There was a spectrum, however, in the end-organ response to Ang I during ACE inhibition. Responses of plasma aldosterone concentration and blood pressure were in excellent accord with the reduction in Ang II formation. On the other hand, responses of the renal blood supply were substantially less inhibited than anticipated. Under the conditions of this study, ACE inhibition led to nonuniform changes in the response to exogenous Ang I, suggesting intrarenal conversion of Ang I to Ang II.
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Hollenberg et al. (2000) studied Healthy (n=10). Enalapril and Angiotensin I infusion vs. Baseline (before ACE inhibition) was evaluated on Pressor, renal vascular, and adrenal responses to Ang I infusion. ACE inhibition with enalapril led to nonuniform changes in end-organ responses to exogenous Angiotensin I, suggesting intrarenal conversion of Ang I to Ang II.
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