Related Experiment Video

Updated: Oct 2, 2026

Cardiac Pressure-Volume Loop Analysis Using Conductance Catheters in Mice
08:15

Cardiac Pressure-Volume Loop Analysis Using Conductance Catheters in Mice

Published on: September 17, 2015

Different aortic reflection wave responses following long-term angiotensin-converting enzyme inhibition and

B M Pannier1, A P Guerin, S J Marchais

  • 1Centre Hospitalier FH Manhes, Fleury-Mérogis, France.

Clinical and Experimental Pharmacology & Physiology
|March 21, 2002
PubMed

Insights

Both perindopril (an ACE inhibitor) and atenolol (a beta-blocker) effectively lower blood pressure in hypertensive patients. Perindopril uniquely reduced arterial wave reflections, while atenolol more significantly improved aortic stiffness.

Area of Science:

  • Cardiology
  • Pharmacology
  • Vascular Physiology

Background:

  • Arterial hypertension is characterized by elevated central systolic and pulse pressures, influenced by aortic wave reflections.
  • Understanding the impact of antihypertensive medications on these hemodynamic parameters is crucial for effective treatment.

Purpose of the Study:

  • To assess central pressure alterations in the carotid artery after 1 month of treatment with perindopril or atenolol.
  • To investigate hemodynamic changes within 8 hours of drug intake.

Main Methods:

  • A double-blind, randomized cross-over study involving 20 hypertensive patients.
  • Comparison of perindopril (ACE inhibitor) and atenolol (beta-blocker) over 4-week treatment periods.
  • Serial measurements of brachial and carotid artery pressures, pulse wave velocity, and aortic wave reflections.

Main Results:

  • Both perindopril and atenolol reduced brachial and carotid artery pressures.
  • Atenolol decreased heart rate and pulse wave velocity more significantly than perindopril.
  • Perindopril significantly reduced arterial wave reflections, an effect not observed with atenolol.

Conclusions:

  • Both ACE inhibitors and beta-blockers improve central pulse pressure in hypertension.
  • Perindopril uniquely reduces arterial wave reflections, while atenolol demonstrates a greater effect on aortic stiffness.
  • These distinct mechanisms contribute to improved central hemodynamics in hypertensive patients.

Related Concept Videos

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...
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...
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: Action of β1 Blockers01:17

Antihypertensive Drugs: Action of β1 Blockers

β1-receptors are primarily located in the heart and kidneys. In cardiac myocytes, these receptors interact with neurotransmitters released by the sympathetic nervous system during heightened activity or danger. As a result, β1-receptors get activated, initiating a series of biochemical processes. Excessive activation of beta receptors due to chronic stress can abnormally increase heart rate and contractility, resulting in high blood pressure or hypertension. To counteract this, β1-blockers...
Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
Adrenergic Antagonists: ɑ and β-Receptor Blockers01:31

Adrenergic Antagonists: ɑ and β-Receptor Blockers

Third-generation β-blockers, such as labetalol and carvedilol, represent a significant advancement in managing cardiovascular conditions. Unlike conventional β-blockers, which can induce peripheral vasoconstriction, third-generation drugs block α1 adrenoceptors. This promotes vasodilation through several mechanisms, such as increased nitric oxide production, inhibition of calcium ion entry, opening of potassium ion channels, and antioxidant action. Labetalol, for instance, is clinically...