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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

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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: 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,...
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Hypertension is a chronic condition in which the blood's force against artery walls is excessively high, posing risks such as heart disease. The condition's underlying mechanisms involve complex interactions among the cardiovascular, kidney, and autonomic nervous systems.Renin-Angiotensin-Aldosterone System (RAAS): This system significantly influences blood pressure regulation. When blood pressure decreases, the kidneys secrete renin. This enzyme transforms angiotensinogen, a plasma protein,...
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Related Experiment Video

Updated: May 12, 2026

Assessing Endothelial Vasodilator Function with the Endo-PAT 2000
07:46

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Published on: October 15, 2010

Angiotensin-converting enzyme 2 activation improves endothelial function.

Rodrigo A Fraga-Silva1, Fabiana P Costa-Fraga, Tatiane M Murça

  • 1National Institute of Science and Technology in Nanobiopharmaceutics, Federal University of Minas Gerais, Av. Antônio Carlos, 6627, 31.270-901 Belo Horizonte, MG, Brazil.

Hypertension (Dallas, Tex. : 1979)
|April 24, 2013
PubMed
Summary

Activating angiotensin-converting enzyme 2 (ACE2) with XNT improves endothelial function by reducing oxidative stress in hypertensive and diabetic models. This therapeutic approach targets cardiovascular disease by enhancing vascular health.

Keywords:
angiotensin-(1–7)diabetes mellitusendothelium dysfunctionoxidative stressrenin–angiotensin system

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Last Updated: May 12, 2026

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Area of Science:

  • Cardiovascular Science
  • Pharmacology
  • Endothelial Biology

Background:

  • Endothelial dysfunction involves reduced nitric oxide and increased reactive oxygen species (ROS).
  • The protective renin-angiotensin system axis (ACE2/Ang-(1-7)/Mas) offers vascular benefits.
  • Hypothesis: ACE2 activation can improve endothelial function by decreasing ROS.

Purpose of the Study:

  • To investigate the effects of XNT, a novel ACE2 activator, on endothelial function.
  • To determine if XNT attenuates oxidative stress and improves vascular health in disease models.

Main Methods:

  • In vivo studies using spontaneously hypertensive and diabetic rats treated with XNT.
  • In vitro experiments with rat aortic rings and human aortic endothelial cells.
  • Assessment of vasorelaxant responses and ROS production.
  • Utilized Mas receptor antagonist and knockout models.

Main Results:

  • XNT treatment improved endothelial function in hypertensive and diabetic rats.
  • XNT induced endothelial-dependent vasorelaxation mediated by the Mas receptor.
  • XNT reduced ROS production in vivo and in vitro.
  • XNT attenuated Angiotensin II-induced ROS in human aortic endothelial cells.

Conclusions:

  • Chronic XNT administration improves endothelial function in hypertensive and diabetic models by reducing oxidative stress.
  • XNT-induced vasorelaxation is mediated by the Mas receptor.
  • ACE2 activation represents a promising therapeutic target for cardiovascular diseases.