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Influence of captopril on the arterial baroreceptor reflex in patients with heart failure
K J Osterziel1, N Röhrig, R Dietz
1Department of Internal Medicine, (Cardiology), Ruprecht-Karls-University, Heidelberg, Federal Republic of Germany.
Insights
Captopril enhances the baroreceptor reflex in heart failure patients, increasing sensitivity to heart rate slowing. This effect is independent of blood pressure changes and mediated by increased vagal tone.
Area of Science:
- Cardiovascular Physiology
- Pharmacology
- Nephrology
Background:
- Heart failure (HF) affects cardiovascular regulation, including the baroreceptor reflex.
- The carotid sinus baroreceptor reflex plays a crucial role in maintaining blood pressure homeostasis.
- Angiotensin-converting enzyme inhibitors (ACEIs) like captopril are used in HF management.
Purpose of the Study:
- To investigate the effect of a single captopril dose on carotid sinus baroreceptor reflex sensitivity in male patients with heart failure (NYHA II-III).
- To determine if captopril alters reflex heart rate slowing or blood pressure responses to baroreceptor stimulation.
- To elucidate the mechanism underlying captopril's influence on baroreflex sensitivity.
Main Methods:
- 16 male patients with heart failure (NYHA II-III) received a single 25 mg dose of captopril.
- Carotid sinus baroreceptors were stimulated using an airtight neck chamber.
- Two indices of baroreflex sensitivity were calculated: sensitivity to reflex heart rate slowing and blood pressure response to neck suction.
Main Results:
- Captopril significantly reduced blood pressure (11 ± 1.7 mm Hg) but did not alter heart rate.
- Sensitivity to reflex heart rate slowing increased significantly after captopril administration (from -2.9 ± 0.7 to -5.0 ± 1.3 ms/mmHg).
- The increase in heart rate slowing sensitivity was more pronounced in patients with higher initial sensitivity and was independent of hemodynamic changes.
Conclusions:
- Captopril selectively augments the reflex bradycardia mediated by increased vagal efferent tone in heart failure patients.
- The observed enhancement of baroreflex sensitivity is dependent on the initial reflex sensitivity and not solely due to hemodynamic effects.
- Captopril's influence on baroreflexes may contribute to its therapeutic benefits in heart failure management.
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 pressure fell significantly by 11 +/- 1.7 mm Hg (P less than 0.001), whereas heart rate remained unchanged (85 +/- 3 vs. 83 +/- 3 beats min-1). 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 mmHg-1 (P less than 0.02). 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 less than 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.
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