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Related Concept Videos

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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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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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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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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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: Action of β1 Blockers01:17

Antihypertensive Drugs: Action of β1 Blockers

306
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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Related Experiment Video

Updated: Jun 3, 2025

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors
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APOL1 Modulates Renin-Angiotensin System.

Vinod Kumar1,2, Prabhjot Kaur1,2, Kameshwar Ayasolla1

  • 1Department of Medicine and Feinstein Institute for Medical Research, Zucker School of Medicine, Hempstead, NY 11549, USA.

Biomolecules
|January 8, 2025
PubMed
Summary
This summary is machine-generated.

MicroRNA 193a (miR193a) activates the renin-angiotensin system (RAS) and damages kidney podocytes in APOL1-related kidney disease. Inhibiting miR193a may protect against FSGS by restoring Vitamin D receptor (VDR) and podocyte markers.

Keywords:
APOL1BASP1VDRWT1miR193apodocyterenin-angiotensin system

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Area of Science:

  • Nephrology
  • Molecular Biology
  • Genetics

Background:

  • APOL1 risk alleles (G1, G2) increase susceptibility to Focal Segmental Glomerulosclerosis (FSGS).
  • The renin-angiotensin system (RAS) and microRNAs play roles in kidney injury.
  • Vitamin D receptor (VDR) and Wilms Tumor 1 (WT1) are crucial for podocyte function.

Purpose of the Study:

  • To investigate the role of miR193a in activating RAS and its impact on podocyte injury in the context of APOL1 risk alleles.
  • To explore the regulatory relationship between miR193a, VDR, WT1, and podocyte molecular markers.

Main Methods:

  • Differentiated podocytes (DPDs) expressing different APOL1 variants (G0, G1, G2) were analyzed for renin, VDR, and podocyte molecular markers (PDMMs).
  • Gene expression (mRNA) and protein levels of RAS components, VDR, WT1, and other key proteins were assessed.
  • Bioinformatics, luciferase assays, and studies in miR193a transgenic mice were conducted to confirm regulatory interactions.

Main Results:

  • APOL1 G1/G2 podocytes showed increased renin and RAS components but decreased VDR and WT1 compared to G0 podocytes.
  • miR193a directly targets VDR, leading to reduced VDR expression and increased renin in podocytes.
  • miR193a transgenic mice exhibited elevated blood Angiotensin II (Ang II) levels, reduced VDR and PDMMs, and increased renin in podocytes.

Conclusions:

  • miR193a promotes kidney injury in APOL1-associated FSGS by activating the RAS via VDR and WT1 modulation.
  • Targeting miR193a may offer a therapeutic strategy for APOL1-mediated kidney diseases.