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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...

Antihypertensive Drugs: Angiotensin II Receptor Blockers

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 Inhibitors

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 Inhibitors

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...

Heart Failure Drugs: Diuretics

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...

Antihypertensive Drugs: Vasodilators

Antihypertensive Drugs: Vasodilators

Vasodilators, primarily affecting the smooth muscles within arterial and venous walls, are commonly used for hypertension treatment. Medications such as minoxidil and hydralazine primarily target arteries and arterioles, while sodium nitroprusside acts on arterioles and venules. Minoxidil, functioning as a prodrug, is metabolized by hepatic sulfotransferase into its active form, minoxidil sulfate, after oral administration. This metabolite binds to the sulfonylurea receptor (SUR) component of...

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Related Experiment Video

Updated: Jun 3, 2026

5/6th Nephrectomy in Combination with High Salt Diet and Nitric Oxide Synthase Inhibition to Induce Chronic Kidney Disease in the Lewis Rat

5/6th Nephrectomy in Combination with High Salt Diet and Nitric Oxide Synthase Inhibition to Induce Chronic Kidney Disease in the Lewis Rat

Published on: July 3, 2013

Losartan protects mesenteric arteries from ROS-associated decrease in myogenic constriction following 5/6

Peter Vavrinec¹, Richard Pe van Dokkum, Maaike Goris

¹Department of Clinical Pharmacology, Groningen University Institute for Drug Exploration (GUIDE), University Medical Center Groningen, Groningen, The Netherlands. p.vavrinec@med.umcg.nl

Journal of the Renin-Angiotensin-Aldosterone System : JRAAS

|March 12, 2011

Summary

This summary is machine-generated.

Losartan treatment improved myogenic constriction in chronic renal failure rats by reducing blood pressure and proteinuria. Reactive oxygen scavengers aided constriction in untreated rats, highlighting the roles of the renin-angiotensin-aldosterone system and ROS in CRF vascular dysfunction.

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Area of Science:

Nephrology
Vascular Physiology
Pharmacology

Background:

Chronic renal failure (CRF) is linked to hypertension, proteinuria, and impaired mesenteric artery myogenic constriction (MC).
Reactive oxygen species (ROS) production increases in CRF.
Angiotensin-converting enzyme (ACE) inhibitors show efficacy in slowing disease progression.

Purpose of the Study:

To investigate if losartan (LOS), an angiotensin II type 1 receptor antagonist, prevents MC loss in a rat model of CRF.
To determine if acute ROS scavengers can improve MC in CRF.

Main Methods:

Rats underwent 5/6 nephrectomy (5/6 Nx) and received vehicle or LOS (20 mg/kg/day) for 12 weeks.
Mesenteric artery MC was assessed with and without tempol and catalase.
Systolic blood pressure and proteinuria were monitored weekly.

Main Results:

LOS treatment significantly reduced systolic blood pressure and proteinuria compared to untreated 5/6 Nx rats.
MC was significantly improved in 5/6 Nx + LOS rats (32.3%) versus 5/6 Nx rats (8.9%).
Tempol + catalase enhanced MC in 5/6 Nx rats but not in 5/6 Nx + LOS rats.

Conclusions:

Losartan effectively preserves myogenic constriction in mesenteric arteries of rats with chronic renal failure.
The renin-angiotensin-aldosterone system (RAAS) and ROS play significant roles in systemic vascular dysfunction associated with CRF.