Related Experiment Video

Updated: Jun 9, 2026

A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis
08:21

A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis

Published on: October 26, 2020

Should all hypertensive dialysis patients receive a blocker of the Renin-Angiotensin system?

Arjun D Sinha1, Rajiv Agarwal

  • 1Veterans Affairs Medical Center, 111N, 1481 West 10th Street, Indianapolis, IN 46202, USA.

Current Hypertension Reports
|September 8, 2010
PubMed

Insights

Renin-angiotensin-aldosterone system (RAAS) blockers show mixed results for cardiovascular events in dialysis patients. While some studies suggest benefits, current evidence doesn't support universal recommendation for hypertensive dialysis patients.

Area of Science:

  • Nephrology
  • Cardiology
  • Pharmacology

Background:

  • Hypertension and cardiovascular mortality are prevalent in dialysis patients.
  • Antihypertensive pharmacotherapy may reduce cardiovascular events in this population.
  • Blockers of the renin-angiotensin-aldosterone system (RAAS) are considered due to benefits in other patient groups.

Purpose of the Study:

  • To evaluate the efficacy of RAAS blockers in improving cardiovascular outcomes in dialysis patients.
  • To assess the impact of RAAS blockers on surrogate end points like left ventricular mass.

Main Methods:

  • Review of meta-analyses and clinical trials examining RAAS blockers in hemodialysis and peritoneal dialysis patients.
  • Analysis of data on cardiovascular events and surrogate end points.

Main Results:

  • Evidence for RAAS blockers improving surrogate end points is mixed.
  • One meta-analysis showed improved left ventricular mass in hemodialysis patients.
  • Trials examining cardiovascular events in dialysis patients yielded no significant benefit; hyperkalemia risk appears low.

Conclusions:

  • Current evidence does not support a universal recommendation for RAAS blockers in all hypertensive dialysis patients.
  • Further adequately powered clinical trials are needed to clarify the role of RAAS blockers in this population.

More Related Videos

Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion08:35

Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion

Published on: May 26, 2022

Related Concept Videos

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,...
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...
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: Types of β-Blockers01:28

Antihypertensive Drugs: Types of β-Blockers

β receptors are classified into three subclasses: β1, β2, and β3. β1 receptors are primarily located in the heart and kidneys. When they get activated, they increase heart rate, contractility, and renin release. This process enhances blood pressure and aids in stress management. In contrast, β2 receptors are situated mainly in the lungs, blood vessels, and skeletal muscles. Upon activation, they trigger smooth muscle relaxation, causing bronchodilation and vasodilation. This widens airways and...