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相关概念视频

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 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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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

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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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相关实验视频

Updated: Jun 3, 2025

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors
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APOL1调节了氨酸-氨酸系统.

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
概括

微RNA 193a (miR193a) 激活氨酸酶系统 (RAS),并在与APOL1相关的病中损害细胞. 抑制miR193a可以通过恢复维生素D受体 (VDR) 和 podocyte标记物来保护FSGS.

关键词:
这就是APOL1的原因.在BASP1中使用BASP.这是VDR VDR.在WT1中,WT1就是WT1.在 miR193a 中使用.这是一个podocyte.氨酸 - ангиотензин 系统

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科学领域:

  • 腎臟病學 (nephrology) 是一種醫學.
  • 分子生物学分子生物学
  • 遗传学 遗传学 是一个

背景情况:

  • APOL1风险基因 (G1,G2) 增加了对焦点细分细胞凝结症 (FSGS) 的敏感性.
  • 氨酸-血管激素系统 (RAS) 和微RNA在损伤中起作用.
  • 维生素D受体 (VDR) 和威尔姆斯瘤1 (WT1) 对细胞功能至关重要.

研究的目的:

  • 调查miR193a在激活RAS中的作用及其在APOL1风险等位基因背景下对细胞损伤的影响.
  • 探索 miR193a,VDR,WT1 和 podocyte 分子标记物之间的调控关系.

主要方法:

  • 对表达不同APOL1变体 (G0,G1,G2) 的分化受体细胞 (DPD) 进行了宁,VDR和受体细胞分子标记物 (PDMM) 的分析.
  • 评估了基因表达 (mRNA) 和RAS成分,VDR,WT1和其他关键蛋白质的蛋白质水平.
  • 进行了生物信息学,化酶测定和对miR193a转基因小鼠的研究,以证实调控相互作用.

主要成果:

  • 与G0 podocytes相比,APOL1 G1/G2 podocytes显示了蛋白和RAS成分的增加,但VDR和WT1的减少.
  • miR193a直接向VDR,导致VDR表达减少和细胞中的蛋白增加.
  • miR193a转基因小鼠表现出血液中的 ангиотензин II (Ang II) 水平升高,VDR和PDMMs降低,并且细胞中的蛋白增加.

结论:

  • miR193a通过通过VDR和WT1调制激活RAS来促进APOL1相关的FSGS中的损伤.
  • 针对miR193a可能为APOL1介导的脏疾病提供治疗策略.