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Related Concept Videos

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

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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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Antihypertensive Drugs: Angiotensin II Receptor Blockers01:30

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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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Antihypertensive Drugs: Action of β1 Blockers01:17

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,...
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Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

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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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Antihypertensive Drugs: Direct Renin Inhibitors01:25

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,...
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Hormonal Regulation01:33

Hormonal Regulation

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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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Related Experiment Video

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Assessing Murine Resistance Artery Function Using Pressure Myography
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UBR1 Promotes Sex-Dependent ACE2 Ubiquitination in Hypertension.

Mona Elgazzaz1,2,3,4, Navya Lakkappa1,2,3, Clara Berdasco1,2,3

  • 1Cardiovascular Center of Excellence (M.E., N.L., C.B., U.P.M., A.N., L.R., A.M., A.S., J.J.G., S.S., J.X., X.Y., C.M.F., E.L.), New Orleans, LA.

Hypertension (Dallas, Tex. : 1979)
|November 27, 2024
PubMed
Summary

Ubiquitin protein ligase E3 component N-recognin (UBR1) targets the antihypertensive enzyme angiotensin-converting enzyme 2 (ACE2) for degradation, contributing to hypertension. Targeting UBR1 may restore ACE2 function and treat hypertension.

Keywords:
angiotensin-converting enzyme 2blood pressureestrogenshypertensionhypothalamus

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Hypertension Research

Background:

  • Angiotensin II (Ang-II) impairs angiotensin-converting enzyme 2 (ACE2) function, promoting hypertension.
  • Few ACE2 ubiquitination partners are known, and their role in hypertension is unclear.

Purpose of the Study:

  • Identify ACE2 ubiquitination partners in hypertensive mice.
  • Investigate the role of identified partners in hypertension maintenance.

Main Methods:

  • Proteomics and bioinformatics to identify ACE2 ubiquitination partners.
  • Cell-based validation of UBR1-ACE2 interaction.
  • In vivo UBR1 knockdown in hypertensive male mice.

Main Results:

  • UBR1 identified as an E3 ligase promoting ACE2 ubiquitination and degradation.
  • UBR1 expression is elevated in hypertensive mice and humans, linked to reduced ACE2.
  • UBR1 knockdown restores ACE2 levels and transiently decreases blood pressure in male mice.
  • Testosterone, not estradiol, sex-specifically regulates UBR1.

Conclusions:

  • UBR1 is a novel E3 ubiquitin ligase targeting ACE2 in hypertension.
  • UBR1 and Nedd4-2 may synergistically ubiquitinate ACE2.
  • Targeting UBR1 and Nedd4-2 could restore ACE2 activity in hypertension.