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.

European Heart Journal
|October 1, 1988
PubMed

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.

Related Concept Videos

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
Antihypertensive Drugs: Angiotensin II Receptor Blockers01:30

Antihypertensive Drugs: Angiotensin II Receptor Blockers

In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
Heart Failure Drugs: β-Blockers01:22

Heart Failure Drugs: β-Blockers

β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation, vasodilation, and...
Neural Regulation of Blood Pressure01:18

Neural Regulation of Blood Pressure

The neural regulation of blood pressure involves intricate interactions between the autonomic nervous system (ANS) and cardiovascular system, ensuring adequate perfusion of tissues. This regulation primarily occurs through baroreceptor and chemoreceptor reflexes, involving both short-term and long-term mechanisms.
Baroreceptor Reflex
Baroreceptors, located in the carotid sinuses and aortic arch, detect changes in blood pressure. When blood pressure rises, these stretch-sensitive receptors...
Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...