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. 1985 Jul;20(1):17–25. doi: 10.1111/j.1365-2125.1985.tb02793.x

The effect of captopril on the reflex control heart rate: possible mechanisms.

A A Ajayi, B C Campbell, P A Meredith, A W Kelman, J L Reid
PMCID: PMC1400633  PMID: 2992561

Abstract

Angiotensin converting enzyme inhibitors reduce blood pressure without reflex tachycardia, possibly as a result of enhanced hypothesis that this results from the removal of the parasympathetic activity. We examined the vagolytic action of angiotensin II or alternatively by acetylcholinesterase inhibition. Both captopril and [Sar1ala8] angiotensin II, (saralasin), caused modest falls in blood pressure, without increasing heart rate in normotensive subjects. Captopril and saralasin significantly attenuated the vagally mediated heart rate slowing after facial immersion in water. There was a close correlation between the effects produced by captopril and saralasin on the diving reflex. Infusion of subpressor doses of angiotensin II, reversed the hypotensive effect of captopril and returned the bradycardia after facial immersion to placebo level. In vitro neither captopril nor enalapril or lisinopril affected bovine erythrocyte acetylcholinesterase activity. The parasympathetic effect of angiotensin converting enzyme inhibitors appear to reflect a direct consequence of the removal of angiotensin II.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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