贝塔1-上腺素受体阻断减弱了血管新生素II介导的甲醇胺释放到心脏间歇体中,在心肌吐中
José Tallaj1, Chih-Chang Wei, Gerald H Hankes
1Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA.
Circulation
|July 9, 2003
概括
贝塔1-上腺体受体阻塞减少心脏的上腺素和上腺素释放在上腺回的狗. 这种治疗减弱了血管新素II介导的交感刺激,并在早期体积过载时降低了心脏血管新素转化酶的表达.
科学领域:
- 心血管生理学心血管生理学
- 药理学 药理学是指药理学的学科.
- 脏系统 脏系统
背景情况:
- 副心脏反 (MR) 可能导致心脏功能障碍.
- 氨酸-动脉素系统 (RAS) 在心血管调节中发挥作用.
- 贝塔-1上腺素受体参与了同情神经系统的活动.
研究的目的:
- 为了调查β1-上腺受体阻塞是否影响血管素II (Ang II) 诱导的心脏中上腺素 (NE) 和上腺素 (Epi) 的释放.
- 为了检查β1受体阻塞对心脏NE和Epi水平的影响,在一只狗模型中进行了额头吐.
主要方法:
- 使用了一种实验诱导的头回 (MR) 的狗模型.
- 患有MR的狗被用β1受体阻断剂 (metoprolol succinate) 治疗.
- 输注 ангиотензин II 以评估 NE 和 Epi 释放到心脏间歇性液体 (ISF) 和循环中.
主要成果:
- 在MR犬的血Ang II水平显著增加.
- 在MR犬中,Ang II输液增加了ISF和循环NE和Epi.
- 在MR犬中,β1受体阻塞使NE和Epi水平恢复到正常水平,并降低了心脏血管酶转化酶活性.
结论:
- 贝塔1受体阻塞有效地减少了RAS介导的同情刺激在早期的MR.
- 治疗减弱了Ang II诱导的NE和Epi释放到心脏ISF和血液循环中.
- 在体积过载时,β1受体阻塞会降低心脏血管氨转化酶的表达.
更多相关视频
相关概念视频
01:17Antihypertensive Drugs: Action of β1 Blockers
2.2K
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,...
2.2K
01:30Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors
2.7K
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...
2.7K
01:30Antihypertensive Drugs: Angiotensin II Receptor Blockers
2.9K
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...
2.9K
01:26Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
1.9K
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...
1.9K
01:20Mitral Regurgitation I: Introduction
1.3K
Mitral regurgitation is characterized by the backward circulation of blood from the left ventricle to the left atrium during systole, a phase of the cardiac cycle when the heart contracts and pumps blood out of the chambers. This abnormal flow occurs primarily due to the dysfunction of the mitral valve or its supporting structures, which include the mitral leaflets, chordae tendineae, annulus, and papillary muscles.Etiology and Mechanisms:Primary Mitral Regurgitation: This type arises from...
1.3K
01:25Mitral Regurgitation III: Medical Management
686
Mitral regurgitation (MR) is characterized by retrograde blood circulation from the left ventricle into the left atrium due to inadequate mitral valve closure. The severity of the condition, symptoms, and underlying cause determine treatment strategies.Monitoring and Pharmacological TreatmentPatients with mild to moderate MR typically do not need immediate intervention but regular monitoring to assess progression and guide treatment. Patients with mild MR should have an echocardiogram every 3-5...
686