Related Experiment Video

Updated: Jun 10, 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

Does blockade of the Renin-Angiotensin-aldosterone system slow progression of all forms of kidney disease?

Michael R Lattanzio1, Matthew R Weir

  • 1Division of Nephrology, University of Maryland School of Medicine Medical Center, 22 South Greene Street, Room N3W143, Baltimore, MD 21201, USA.

Current Hypertension Reports
|August 13, 2010
PubMed

Insights

Blocking the renin-angiotensin-aldosterone system (RAAS) can slow chronic kidney disease (CKD) progression. This review examines evidence for RAAS blockade across various CKD types.

Area of Science:

  • Nephrology
  • Pharmacology
  • Internal Medicine

Background:

  • Chronic kidney disease (CKD) progression is influenced by various factors.
  • Activation of the renin-angiotensin-aldosterone system (RAAS) is a key mechanism accelerating CKD.
  • Current evidence for RAAS blockade in diverse CKD forms is limited.

Purpose of the Study:

  • To review current evidence on RAAS blockade for slowing CKD progression.
  • To assess the efficacy of RAAS blockade across different CKD etiologies.
  • To highlight the role of RAAS in CKD pathophysiology.

Main Methods:

  • Literature review of studies on RAAS blockade in CKD.
  • Analysis of evidence for angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, mineralocorticoid receptor antagonists, and direct renin inhibitors.
  • Synthesis of data regarding RAAS blockade's impact on CKD progression rates.

Main Results:

  • RAAS activation is a common pathway in CKD progression.
  • Pharmacological interruption of RAAS shows potential in slowing CKD.
  • Evidence supporting a generalized approach is still developing.

Conclusions:

  • RAAS blockade is a promising strategy for managing CKD progression.
  • Further evidence-based data is needed to guide universal application.
  • Targeting RAAS is crucial for mitigating CKD advancement.

More Related Videos

5/6 Nephrectomy Using Sharp Bipolectomy Via Midline Laparotomy in Rats05:34

5/6 Nephrectomy Using Sharp Bipolectomy Via Midline Laparotomy in Rats

Published on: April 4, 2025

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,...
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: 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: Potassium-Sparing Diuretics01:28

Antihypertensive Drugs: Potassium-Sparing Diuretics

Liddle syndrome is a genetically inherited form of hypertension characterized by the overactivity of epithelial sodium channels in the nephron, the functional unit of the kidney. This heightened activity leads to increased sodium reabsorption and excessive excretion of potassium. To counteract this, potassium-sparing diuretics such as amiloride are used. They function by blocking these sodium channels, thereby reducing the influx of sodium into the epithelial cells and minimizing the loss of...
Chronic Kidney Disease III: Interprofessional Care01:28

Chronic Kidney Disease III: Interprofessional Care

Chronic kidney disease (CKD) requires collaborative and comprehensive management. CKD progresses through stages and can lead to end-stage kidney disease (ESKD) if untreated. Interprofessional collaboration and patient education are crucial, enabling patients to manage their health and improve their quality of life.Diagnostic approach for chronic kidney diseaseThe diagnosis of CKD primarily focuses on the glomerular filtration rate (GFR), which assesses kidney function by measuring how well...