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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,...
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...
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: Potassium-Sparing Diuretics01:28

Antihypertensive Drugs: Potassium-Sparing Diuretics

Liddle syndrome is a genetically inherited form of hypertension characterized by the overactivity of epithelial sodium channels in the nephron, the functional unit of the kidney. This heightened activity leads to increased sodium reabsorption and excessive excretion of potassium. To counteract this, potassium-sparing diuretics such as amiloride are used. They function by blocking these sodium channels, thereby reducing the influx of sodium into the epithelial cells and minimizing the loss of...
Heart Failure Drugs: Diuretics01:22

Heart Failure Drugs: Diuretics

Heart failure and kidney perfusion are interconnected in a complex way. Reduced renal perfusion and venous congestion are two significant factors that contribute to renal dysfunction in heart failure. The kidneys, primarily responsible for fluid balance in the body, are adversely affected due to compromised cardiac output and increased venous pressure. In response to reduced renal perfusion, the kidneys activate neurohumoral mechanisms to restore balance. However, these mechanisms can be...

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Related Experiment Video

Updated: May 29, 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

Renin inhibitors.

Naomi D L Fisher1, Emma A Meagher

  • 1Division of Endocrinology, Diabetes and Hypertension, Hypertension Services, Brigham and Women's Hospital, Boston, MA, USA. nfisher@partners.org

Journal of Clinical Hypertension (Greenwich, Conn.)
|September 8, 2011
PubMed
Summary
This summary is machine-generated.

Aliskiren is an oral renin inhibitor for hypertension, showing blood pressure reductions comparable to other agents. It may offer benefits in diabetic nephropathy, but long-term cardiovascular protection data are pending.

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Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion
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A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis
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Published on: October 26, 2020

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

Area of Science:

  • Cardiovascular pharmacology
  • Nephrology
  • Hypertension management

Background:

  • Aliskiren is the only US FDA-approved oral renin inhibitor for hypertension.
  • It demonstrates efficacy in lowering blood pressure, both as monotherapy and in combination with other antihypertensives.

Purpose of the Study:

  • To summarize key points and practical recommendations for aliskiren use.
  • To highlight its role in hypertension management and potential benefits in specific patient populations.

Main Methods:

  • Review of clinical data and evidence regarding aliskiren's efficacy and safety.
  • Analysis of its pharmacokinetic profile and interactions with other antihypertensive agents.

Main Results:

  • Aliskiren offers comparable blood pressure reduction to other agents.
  • Early data suggest benefits in diabetic nephropathy, with cardiovascular outcomes yet to be determined.
  • No initial dose adjustment is needed for elderly or renally impaired patients, though caution is advised in severe impairment or renal artery stenosis.
  • Combining aliskiren with agents that increase plasma renin activity, like thiazide diuretics, ACE inhibitors, and ARBs, is considered rational.
  • A reactive rise in renin occurs with aliskiren, but it is not evidenced as harmful.
  • Adverse events like edema and cough are reported at low rates, comparable to or lower than other agents.

Conclusions:

  • Aliskiren is an effective oral renin inhibitor for hypertension.
  • Its role in diabetic nephropathy warrants further investigation for cardiovascular benefits.
  • Clinical experience guides its use in specific patient groups and in combination therapy.