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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

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: 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,...
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,...
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.
Antihypertensive Drugs: Action of β1 Blockers01:17

Antihypertensive Drugs: Action of β1 Blockers

β1-receptors are primarily located in the heart and kidneys. In cardiac myocytes, these receptors interact with neurotransmitters released by the sympathetic nervous system during heightened activity or danger. As a result, β1-receptors get activated, initiating a series of biochemical processes. Excessive activation of beta receptors due to chronic stress can abnormally increase heart rate and contractility, resulting in high blood pressure or hypertension. To counteract this, β1-blockers...

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Articles linked to this work by shared authors, journal, and citation graph.

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Same author

PRESSOR SUBSTANCES FROM THE BODY FLUIDS OF MAN IN HEALTH AND DISEASE.

The Journal of experimental medicine·2009
Same author

OBSERVATIONS ON THE DEPRESSOR EXTRACTS OF HUMAN BLOOD AND ON THE VASCULAR ACTION OF EXTRACTS OF RABBIT AND DOG BLOOD.

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

The Journal of experimental medicine·2009
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A CRYSTALLINE PRESSOR SUBSTANCE (ANGIOTONIN) RESULTING FROM THE REACTION BETWEEN RENIN AND RENIN-ACTIVATOR.

The Journal of experimental medicine·2009
Same author

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

The Journal of experimental medicine·2009
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THE LIBERATION OF RENIN BY PERFUSION OF KIDNEYS FOLLOWING REDUCTION OF PULSE PRESSURE.

The Journal of experimental medicine·2009

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Updated: Jun 19, 2026

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

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

R G Abell1, I H Page

  • 1Department of Anatomy, Medical School, University of Pennsylvania, Philadelphia, and the Lilly Laboratory for Clinical Research, Indianapolis City Hospital, Indianapolis.

The Journal of Experimental Medicine
|October 30, 2009
PubMed
Summary

Renin and angiotonin cause mild blood vessel constriction in rabbits, unlike epinephrine and pitressin which cause severe vasoconstriction. This study compares the effects of these vasoactive substances on blood flow and vessel diameter.

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Last Updated: Jun 19, 2026

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Published on: May 26, 2022

Area of Science:

  • Pharmacology
  • Physiology
  • Cardiovascular Research

Background:

  • Vasoactive substances play a crucial role in regulating blood pressure and flow.
  • Understanding the differential effects of various agents on the vasculature is essential for cardiovascular research.

Purpose of the Study:

  • To compare the vasoconstrictive effects of renin, angiotonin, tyramine, methylguanidine sulfate, epinephrine, and pitressin on rabbit ear vasculature.
  • To investigate the impact of these agents on arterioles, capillaries, and venules, and their effect on tissue blood flow.

Main Methods:

  • Direct microscopic observation of rabbit ear vasculature (arterioles, capillaries, venules) in vivo.
  • Administration of varying doses of renin, angiotonin, tyramine, methylguanidine sulfate, epinephrine, and pitressin.
  • Assessment of vasoconstriction, duration of effect, and impact on blood flow.

Main Results:

  • Renin and angiotonin (in small doses) caused mild arteriolar constriction with minimal venular constriction and no significant reduction in blood flow.
  • Epinephrine and pitressin induced severe and prolonged arteriolar constriction, significantly reducing or abolishing blood flow.
  • Tyramine and methylguanidine sulfate showed effects similar to renin and angiotonin.

Conclusions:

  • Angiotonin's peripheral vasoconstrictor action is similar to renin's but faster.
  • Epinephrine and pitressin exhibit more potent and sustained vasoconstriction compared to renin and angiotonin.
  • The study highlights differential vascular responses to various vasoactive agents, impacting blood flow regulation.