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Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

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...

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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: Direct Renin Inhibitors

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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 II Receptor Blockers

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Antihypertensive Drugs: Action of β1 Blockers

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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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Related Experiment Video

Updated: Jun 19, 2026

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors

Published on: June 7, 2016

THE CARDIAC FACTOR IN THE "PRESSOR" EFFECTS OF RENIN AND ANGIOTONIN.

W H Hill¹, E C Andrus

¹Department of Medicine, The Johns Hopkins University and Hospital, Baltimore.

The Journal of Experimental Medicine

|October 30, 2009

Summary

Renin and angiotonin increase cardiac output and arterial pressure. Angiotonin uniquely decreases coronary flow but increases heart beat amplitude, with arrhythmias appearing at high blood pressure.

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Last Updated: Jun 19, 2026

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors

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Published on: June 7, 2016

Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion

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Published on: May 26, 2022

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

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

Published on: October 26, 2020

Area of Science:

Cardiovascular Physiology
Renal Hypertension

Background:

Renal pressor substances like renin and angiotonin play a role in blood pressure regulation.
Their direct effects on cardiac function require further elucidation.

Purpose of the Study:

To investigate the direct cardiac effects of renin and angiotonin.
To understand the mechanisms underlying the pressor responses mediated by these substances.

Main Methods:

Isolated cat hearts and Starling heart-lung preparations were used to assess cardiac function.
Electrocardiograms were recorded in anesthetized cats to monitor cardiac rhythm during induced pressor effects.

Main Results:

Angiotonin decreased coronary flow and increased ventricular contractility, while renin had no significant effect on isolated hearts.
Both substances augmented cardiac output and arterial pressure in the heart-lung preparation.
Cardiac arrhythmias occurred at elevated blood pressures (>190 mm Hg) in vivo, preventable by vagotomy or atropine.

Conclusions:

The pressor effects of renal substances involve direct myocardial stimulation and enhanced ventricular contraction.
Increased cardiac output is a consequence of these actions, provided diastolic volume is not excessively reduced.
Vagal nerve activity contributes to the arrhythmogenic potential of pressor substances.