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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,...
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...
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.
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...
Hypertension and Regulation of Blood Pressure01:18

Hypertension and Regulation of Blood Pressure

Hypertension, the most common cardiovascular disease, is diagnosed through repeated measurements of elevated blood pressure. Its risks, including damage to the kidney, heart, and brain, are directly proportional to blood pressure levels. Starting from 115/75 mm Hg, the risk of cardiovascular disease doubles with each increment of 20/10 mm Hg. The diagnosis relies on blood pressure measurements, not on patient symptoms, as hypertension is often asymptomatic until end-organ damage is imminent or...
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...

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THE VASOCONSTRICTOR ACTION OF PLASMA FROM HYPERTENSIVE PATIENTS AND DOGS.

The Journal of experimental medicine·2009
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ON THE NATURE OF THE PRESSOR ACTION OF RENIN.

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ANGIOTONIN-ACTIVATOR, RENIN- AND ANGIOTONIN-INHIBITOR, AND THE MECHANISM OF ANGIOTONIN TACHYPHYLAXIS IN NORMAL, HYPERTENSIVE, AND NEPHRECTOMIZED ANIMALS.

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THE REACTION OF PERIPHERAL BLOOD VESSELS TO ANGIOTONIN, RENIN, AND OTHER PRESSOR AGENTS.

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A CRYSTALLINE PRESSOR SUBSTANCE (ANGIOTONIN) RESULTING FROM THE REACTION BETWEEN RENIN AND RENIN-ACTIVATOR.

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Updated: Jun 19, 2026

Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion
08:35

Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion

Published on: May 26, 2022

THE LIBERATION OF RENIN BY PERFUSION OF KIDNEYS FOLLOWING REDUCTION OF PULSE PRESSURE.

K G Kohlstaedt1, I H Page

  • 1Lilly Laboratory for Clinical Research, Indianapolis City Hospital, Indianapolis.

The Journal of Experimental Medicine
|October 30, 2009
PubMed
Summary
This summary is machine-generated.

Isolated dog kidneys maintain function during perfusion but show low urea clearance. Reduced pulse pressure alters renal venous blood, causing vasoconstriction, unlike hind leg perfusion, indicating kidney-specific responses.

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Last Updated: Jun 19, 2026

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Published on: May 26, 2022

A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis
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06:51

Multilevel Microdissection and Functional-Structural Profiling of Human Renal Arterial Branches

Published on: September 5, 2025

Area of Science:

  • Physiology
  • Renal Physiology
  • Hemodynamics

Background:

  • Isolated organ perfusion is a key technique in physiological research.
  • Understanding renal venous blood composition is crucial for kidney function assessment.

Purpose of the Study:

  • To investigate the functional and biochemical changes in isolated dog kidneys under perfusion.
  • To determine if reduced pulse pressure affects renal venous blood properties.

Main Methods:

  • Isolated dog kidneys were perfused with defibrinated blood under controlled hemodynamic conditions.
  • Pulse pressure was manipulated by constricting the renal artery.
  • Renal venous blood was tested for vasoconstriction properties using an isolated rabbit's ear assay with renin-activator.

Main Results:

  • Isolated kidneys maintained blood flow, urine secretion, and oxygen consumption, but exhibited low urea clearance.
  • Reducing pulse pressure impaired urea clearance and urine secretion, with slight oxygen consumption reduction.
  • Renal venous blood collected after reduced pulse pressure induced intense vasoconstriction, a change not observed in hind leg perfusion.

Conclusions:

  • Isolated canine kidneys can be perfused to maintain physiological parameters, though urea clearance is limited.
  • Reduced renal arterial pulse pressure alters venous blood, generating vasoconstrictive properties specific to the kidney.
  • These findings suggest a kidney-specific response to altered hemodynamics impacting venous blood composition.