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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,...
Hormonal Regulation01:33

Hormonal Regulation

The renin-aldosterone system is an endocrine system which guides the renal absorption of water and electrolytes, thus managing blood pressure and osmoregulation. Activation of the system begins in the kidneys with a small cluster of cells adjacent to the afferent and efferent blood vessels of the renal corpuscle. As the nephrons are filtering blood, juxtaglomerular cells monitor blood pressure. If they detect a decrease in pressure, they release the hormone renin into the bloodstream.
Hypertension II: Pathophysiology01:29

Hypertension II: Pathophysiology

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,...
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...
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Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

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Related Experiment Video

Updated: May 23, 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

(Pro)renin and its receptors: pathophysiological implications.

Wendy W Batenburg1, A H Jan Danser

  • 1Division of Pharmacology and Vascular Medicine, Department of Internal Medicine, Erasmus MC, 3015 GE Rotterdam, The Netherlands.

Clinical Science (London, England : 1979)
|April 13, 2012
PubMed
Summary
This summary is machine-generated.

Tissue renin generation relies on uptake of circulating renin or prorenin. The (pro)renin receptor

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Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors
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Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors

Published on: June 7, 2016

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Last Updated: May 23, 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

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors
12:03

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors

Published on: June 7, 2016

Area of Science:

  • Biochemistry
  • Physiology
  • Molecular Biology

Background:

  • Tissue angiotensin generation is influenced by circulating renin and prorenin uptake.
  • The (pro)renin receptor was proposed as a mediator of this uptake, but its affinity is questionable.
  • Previous candidates for renin uptake include renin-binding protein and M6P/IGF2 receptor.

Purpose of the Study:

  • To review and critically evaluate the role of the (pro)renin receptor in (pro)renin uptake.
  • To compare the (pro)renin receptor with other proposed uptake mechanisms.
  • To discuss the implications of (pro)renin receptor blockade and knockout studies.

Main Methods:

  • Literature review of studies on (pro)renin receptor function and blockade.
  • Analysis of in vitro and in vivo experimental data.
  • Comparison of findings across different studies and proposed mechanisms.

Main Results:

  • In vitro studies show (pro)renin receptor activation leads to profibrotic effects.
  • The (pro)renin receptor blocker HRP showed benefits in diabetic animal models.
  • (Pro)renin receptor knockout studies resulted in lethal, (pro)renin-independent consequences, suggesting a role in vacuolar H+-ATPase stability.

Conclusions:

  • The in vivo interaction between (pro)renin and its receptor may be limited to (pro)renin-synthesizing organs like the kidney.
  • The (pro)renin receptor's proposed role in mediating circulating (pro)renin uptake is uncertain.
  • Further research is needed to clarify the precise function of the (pro)renin receptor and the effects of its blockade.