Jove
Visualize
联系我们
JoVE
x logofacebook logolinkedin logoyoutube logo
关于 JoVE
概览领导团队博客JoVE 帮助中心
作者
出版流程编辑委员会范围与政策同行评审常见问题投稿
图书馆员
用户评价订阅访问资源图书馆顾问委员会常见问题
研究
JoVE JournalMethods CollectionsJoVE Encyclopedia of Experiments存档
教育
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab Manual教师资源中心教师网站
使用条款与条件
隐私政策
政策

相关概念视频

Nitric Oxide Signaling Pathway01:28

Nitric Oxide Signaling Pathway

6.9K
Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure...
6.9K
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

2.9K
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...
2.9K
Antihypertensive Drugs: Angiotensin II Receptor Blockers01:30

Antihypertensive Drugs: Angiotensin II Receptor Blockers

3.1K
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...
3.1K
Antihypertensive Drugs: Vasodilators01:23

Antihypertensive Drugs: Vasodilators

2.5K
Vasodilators, primarily affecting the smooth muscles within arterial and venous walls, are commonly used for hypertension treatment. Medications such as minoxidil and hydralazine primarily target arteries and arterioles, while sodium nitroprusside acts on arterioles and venules. Minoxidil, functioning as a prodrug, is metabolized by hepatic sulfotransferase into its active form, minoxidil sulfate, after oral administration. This metabolite binds to the sulfonylurea receptor (SUR) component of...
2.5K
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

1.5K
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...
1.5K
Hypertension II: Pathophysiology01:29

Hypertension II: Pathophysiology

1.6K
Hypertension is a chronic condition in which the blood's force against artery walls is excessively high, posing risks such as heart disease. The condition's underlying mechanisms involve complex interactions among the cardiovascular, kidney, and autonomic nervous systems.Renin-Angiotensin-Aldosterone System (RAAS): This system significantly influences blood pressure regulation. When blood pressure decreases, the kidneys secrete renin. This enzyme transforms angiotensinogen, a plasma protein,...
1.6K

您也可能阅读

相关文章

通过共同作者、期刊和引用图与本文相关的文章。

排序
Same author

Heart failure with preserved ejection fraction or non-cardiac dyspnea in paroxysmal atrial fibrillation: The role of left atrial strain.

International journal of cardiology·2020
Same author

IgE promotes type 2 innate lymphoid cells in murine food allergy.

Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology·2017
Same author

Wasted septal work in left ventricular dyssynchrony: a novel principle to predict response to cardiac resynchronization therapy.

European heart journal. Cardiovascular Imaging·2016
Same author

Electrical remodeling reflected by QRS and T vector changes following cardiac resynchronization therapy is related to survival in heart failure patients with left bundle branch block.

Journal of electrocardiology·2015
Same author

Epicardial catheter-based ventricular reconstruction (ECVR) in a patient with ischemic heart failure and an anteroapical aneurysm.

Acta clinica Belgica·2014
Same author

Aging and contribution of MyD88 and TRIF to expression of TLR pathway-associated genes following stimulation with Porphyromonas gingivalis.

Journal of periodontal research·2014

相关实验视频

Updated: Apr 14, 2026

Assessing Murine Resistance Artery Function Using Pressure Myography
07:25

Assessing Murine Resistance Artery Function Using Pressure Myography

Published on: June 7, 2013

23.4K

慢性N(G) -nitro-L-arginine甲基诱导的高血压:在没有过度增强的情况下,对缩负荷的新型分子适应.

J Bartunek1, E O Weinberg, M Tajima

  • 1Charles A. Dana Research Institute and the Harvard-Thorndike Laboratory, Beth Israel Deaconess Medical Center, and Department of Medicine, Cardiovascular Division, Harvard Medical School, Boston, MA 02215, USA.

Circulation
|February 2, 2000
PubMed
概括

即使当心脏缩被N(G) -nitro-L-arginine甲基 (L-NAME) 抑制时,心脏也会适应慢性压力过载. 这种适应通过重塑和增强依赖的收缩性来维持缩性.

关键词:
美国宇航局纪律心肺非NASA中心的中心.

更多相关视频

5/6th Nephrectomy in Combination with High Salt Diet and Nitric Oxide Synthase Inhibition to Induce Chronic Kidney Disease in the Lewis Rat
08:50

5/6th Nephrectomy in Combination with High Salt Diet and Nitric Oxide Synthase Inhibition to Induce Chronic Kidney Disease in the Lewis Rat

Published on: July 3, 2013

24.5K
A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis
08:21

A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis

Published on: October 26, 2020

5.8K

相关实验视频

Last Updated: Apr 14, 2026

Assessing Murine Resistance Artery Function Using Pressure Myography
07:25

Assessing Murine Resistance Artery Function Using Pressure Myography

Published on: June 7, 2013

23.4K
5/6th Nephrectomy in Combination with High Salt Diet and Nitric Oxide Synthase Inhibition to Induce Chronic Kidney Disease in the Lewis Rat
08:50

5/6th Nephrectomy in Combination with High Salt Diet and Nitric Oxide Synthase Inhibition to Induce Chronic Kidney Disease in the Lewis Rat

Published on: July 3, 2013

24.5K
A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis
08:21

A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis

Published on: October 26, 2020

5.8K

科学领域:

  • 心血管生理学心血管生理学
  • 心脏适应的过程
  • 高血压研究 高血压研究

背景情况:

  • 甲基 (L-NAME) 抑制氧化的合成,诱导高血压和预期的心脏缩.
  • 尽管持续的压力过载,但L-NAME表现出负面的代谢效应,抑制蛋白质合成和心脏缩.
  • 这项研究研究了当高缩在药理上受到抑制时,心脏适应压力过载的情况.

研究的目的:

  • 测试L-NAME诱导的高血压期间,尽管抑制了高,但心脏适应是否发生.
  • 阐明在没有补偿性心脏生长的情况下适应的机制.
  • 评估左心室 (LV) 缩性表现在严重的慢性压力过载和抑制性缩下维持的情况.

主要方法:

  • 雄性大鼠被给予L-NAME (50毫克/公斤/天) 或安慰剂6周.
  • 测量了缩壁应力,并将L-NAME诱导的高血压和大动脉狭窄模型进行比较.
  • 评估了左心室 (LV) 质量,肌细胞大小和心脏表现.

主要成果:

  • 由L-NAME诱导的高血压导致了可比于大动脉狭窄症的缩性壁应力.
  • 与大动脉狭窄不同,L-NAME治疗没有增加 LV 质量或肌细胞大小,这表明抑制了缩.
  • 尽管抑制了缩,但 LV 系统性表现保持不变,心力衰竭没有发展.

结论:

  • 严重的慢性压力过载与抑制的补偿性缩 (通过L-NAME) 会导致成功的适应.
  • 心脏适应包括左心室 (LV) 改造和增强的依赖的收缩性.
  • 保存的α-和β-肌酸重链表达和SERCA-2有助于维持缩功能.