Copyright © 1988 by the European Society of Cardiology.
© 1988 The European Society of Cardiology
Influence of captopril on the arterial baroreceptor reflex in patients with heart failure
Department of Internal Medicine (Cardiology), Ruprecht-Karls-University Heidelberg, Federal Republic of Germany
Address for reprints: Karl J. Osterziel, M.D., Department of Internal Medicine (Cardiology), Ruprecht-Karls-University, Bergheimer Strasse 58, 6900 Heidelberg, F.R.G.
Abstract
In 16 male patients with heart failure (NYHA II-III), the influence of a single dose of 25 mg captopril on the carotid sinus baroreceptor reflex was examined. Blood presure fell significantly by 11 ± 1.7 mm Hg (P < 0.001), whereas heart rate remained unchanged (85 ± 3 vs. 83 ± 3 beats min1). Carotid sinus baroreceptors were stimulated by means of an airtight neck chamber. Two indices of baroreflex sensitivity were calculated. (1) The sensitivity to reflex heart rate slowing was increased by captopril from 2.9 ± 0.7 to 5.0 ± 1.3 ms mmHg1 (P <0.002). The higher the initial sensitivity the more pronounced was the change after captopril with an increase of sensitivity by 46% (y = 1.46x 0.17, P <0.01). This increase in sensitivity cannot be explained by haemodynamic changes induced by captopril. (2) In eight patients the sensitivity of the baroreflex to increased transmural pressure gradients of the carotid sinus was evaluated by registration of the blood pressure response to neck suction; this demonstrated an unchanged responsiveness following captopril administration. From these data it can be concluded that captopril selectively augments a reflex bradycardia which is mediated by an increase in vagal efferent tone. The change in the reflex response depends on the initial reflex sensitivity and cannot be explained by haemodynamic changes caused by captopril.
Key Words: Captopril heart failure baroreceptors
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