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Related Concept Videos

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

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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...
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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 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,...
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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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Endocrinal or hormonal intervention in the cardiovascular system is predominantly exerted by the catecholamines - epinephrine and norepinephrine, as well as a slew of hormones that interact with renal function to modulate blood volume.
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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.
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Updated: Jan 15, 2026

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors
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Combined RAS Modulation: The Effect on Plasma and Tissue Angiotensin Peptide Levels.

L Paulis1, R Rajkovicova, K Repova

  • 1Institute of Pathophysiology, Faculty of Medicine, Comenius University, Bratislava, Slovak Republic.

Physiological Research
|January 14, 2026
PubMed
Summary
This summary is machine-generated.

Combined renin-angiotensin system (RAS) blockade improves blood pressure but not outcomes. Dual blockade may reduce beneficial Ang 1-7, suggesting a need for cautious therapeutic strategies.

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Area of Science:

  • Cardiovascular Research
  • Pharmacology
  • Hypertension Management

Background:

  • Combined renin-angiotensin system (RAS) inhibition improves blood pressure control but not clinical outcomes.
  • Complex changes in angiotensin peptide profiles are crucial in combined RAS blockade.
  • Spontaneously hypertensive rats (SHR) exhibit hypertension and cardiac hypertrophy.

Purpose of the Study:

  • Investigate hemodynamics and angiotensin peptide profiles in SHR under combined RAS blockade.
  • Evaluate effects of lisinopril, olmesartan, aliskiren, and their dual combinations.
  • Understand the impact on circulating and tissue angiotensin peptides.

Main Methods:

  • Treatment of SHR with lisinopril, olmesartan, aliskiren, and dual combinations.
  • Measurement of hemodynamics, blood pressure, and cardiac morphology.
  • Analysis of circulating and tissue angiotensin peptide profiles (Ang I, Ang II, Ang 1-7).

Main Results:

  • Lisinopril showed the most potent antihypertensive effects, enhanced by combinations.
  • Aliskiren had modest effects in this low-RAS setting.
  • Dual RAS blockade often decreased renal and circulating Ang 1-7 despite hemodynamic efficacy.
  • Left ventricular Ang II primarily derived from circulating sources, while renal peptide synthesis showed local enzymatic activity.

Conclusions:

  • Combined RAS blockade requires a cautious, mechanism-aware approach.
  • Therapeutic strategies should balance blood pressure reduction with Ang 1-7 axis preservation.
  • Understanding tissue-specific peptide synthesis is key for optimizing RAS inhibition.