Related Experiment Video

Updated: May 25, 2026

Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice
07:21

Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice

Published on: September 28, 2015

Protective Role of the ACE2/Ang-(1-9) Axis in Cardiovascular Remodeling

María Paz Ocaranza1, Jorge E Jalil

  • 1Cardiovascular Diseases Division, School of Medicine, Faculty of Medicine, Pontificia Universidad Catolica de Chile, Chile.

International Journal of Hypertension
|February 9, 2012
PubMed

Insights

The ACE2/Ang-(1-9) axis offers a novel therapeutic target for cardiovascular disease. Activating this axis shows promise in protecting the heart and vessels from adverse remodeling in hypertension and heart failure.

Area of Science:

  • Cardiovascular Research
  • Pharmacology
  • Renin-Angiotensin System

Background:

  • Cardiovascular disease (CVD) remains a leading cause of mortality worldwide, despite current treatments.
  • Existing renin-angiotensin system (RAS) blockade therapies for hypertension and heart failure leave significant residual risk and end-organ damage.
  • Novel therapeutic strategies are needed to address persistent cardiovascular remodeling and risk.

Purpose of the Study:

  • To review experimental evidence on the protective role of the ACE2/Ang-(1-9) axis.
  • To evaluate the ACE2/Ang-(1-9) axis as a target for counterbalancing the pro-vasoconstrictive RAS axis.
  • To explore its potential in mitigating adverse cardiovascular remodeling.

Main Methods:

  • Review of current experimental data and literature.
  • Analysis of the biochemical properties of Ang-(1-9) compared to Ang-(1-7).
  • Examination of the interaction of Ang-(1-9) with the Ang II type 2 receptor.

Main Results:

  • The ACE2/Ang-(1-9) axis presents a new target to oppose the vasoconstrictive/proliferative RAS axis.
  • Ang-(1-9) exhibits slower hydrolysis than Ang-(1-7) and can bind the Ang II type 2 receptor.
  • Experimental evidence suggests ACE2/Ang-(1-9) axis activation protects the heart and vessels from adverse remodeling.

Conclusions:

  • Activation of the ACE2/Ang-(1-9) axis demonstrates cardioprotective and vasculoprotective effects.
  • This axis is a promising therapeutic target for managing cardiovascular remodeling in hypertension and heart failure.
  • Potential benefits may extend to renal protection.

More Related Videos

Evaluation of Vascular Control Mechanisms Utilizing Video Microscopy of Isolated Resistance Arteries of Rats10:28

Evaluation of Vascular Control Mechanisms Utilizing Video Microscopy of Isolated Resistance Arteries of Rats

Published on: December 5, 2017

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-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 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...
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,...
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...