ангиотензин转化酶抑制剂和 ангиотензин-II受体对抗剂调节基于内源性清除的处理
Marcin Cwynar1, Katarzyna Stolarz-Skrzypek2, Jerzy Gąsowski3
1Department of Internal Medicine and Gerontology, Jagiellonian University Medical College, Kraków, Poland. marcincw@poczta.onet.pl.
Kardiologia polska
|January 17, 2024
概括
抗胰岛素转化酶抑制剂 (ACE-I) 或抗胰岛素II受体对抗剂 (ARB) 治疗对的处理有不同的影响,这取决于基线近接管中的再吸收. 长期使用ACE-I/ARB可调节具有较低再吸收率的个体的再吸收.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學.
- 心血管医学 心血管医学
- 药理学 药理学是指药理学的学科.
背景情况:
- 近管中的再吸收增加与高血压,肥胖和糖尿病有关.
- 从历史上看,清除率的评估表明了这种关联.
研究的目的:
- 为了研究血管新素转化酶抑制剂 (ACE-I) 和血管新素-II受体对抗剂 (ARB) 对的处理的影响.
- 探讨肥胖个体中摄入量,近接管内再吸收 (FPRNa) 和ACE-I/ARB治疗之间的关系.
主要方法:
- 研究了351名白种人没有尿液治疗和典型的消费.
- 使用内源性清除评估了近端 (FPRNa) 和远端 (FDRNa) 管道的再吸收.
- 通过24小时尿路分泌 (UNaV) 测量每日摄入量.
主要成果:
- 在整个人群中,在FPRNa和ACE-I/ARB治疗之间发现了显著的负相关性.
- 在FPRNa低于中位数的受试者中,ACE-I/ARB治疗与FPRNa有着强烈的不良关系.
- 在FPRNa高于中位数的受试者中,ACE-I/ARB治疗没有显示出与FPRNa的显著关联,但年龄有.
结论:
- 长期的ACE-I/ARB治疗会影响近道管中的再吸收 (FPRNa).
- 这种调节在具有较低基线FPRNa的个体中是显而易见的,但在具有高于中位数FPRNa的个体中并非如此.
- 研究结果表明,ACE-I/ARB对处理的作用因个人再吸收能力而有差异.
相关概念视频
Antihypertensive Drugs: Potassium-Sparing Diuretics
563
Liddle syndrome is a genetically inherited form of hypertension characterized by the overactivity of epithelial sodium channels in the nephron, the functional unit of the kidney. This heightened activity leads to increased sodium reabsorption and excessive excretion of potassium. To counteract this, potassium-sparing diuretics such as amiloride are used. They function by blocking these sodium channels, thereby reducing the influx of sodium into the epithelial cells and minimizing the loss of...
563
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
432
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...
432
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors
645
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...
645
Antihypertensive Drugs: Angiotensin II Receptor Blockers
734
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...
734
Regulation of Sodium and Potassium
538
The regulation of sodium and potassium ion concentrations in the human body is a complex process governed primarily by hormones such as aldosterone, antidiuretic hormone (ADH), and atrial natriuretic peptide (ANP).
Sodium Regulation
Sodium ions make up approximately 90% of extracellular cations, with a normal blood plasma concentration of 136–148 mEq/L. A decrease in blood volume and pressure triggers the release of renin from granular cells in the juxtaglomerular complex (JGC), primarily...
Sodium Regulation
Sodium ions make up approximately 90% of extracellular cations, with a normal blood plasma concentration of 136–148 mEq/L. A decrease in blood volume and pressure triggers the release of renin from granular cells in the juxtaglomerular complex (JGC), primarily...
538
Antihypertensive Drugs: Direct Renin Inhibitors
631
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,...
631


