Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Antihypertensive Drugs: Action of β1 Blockers01:17

Antihypertensive Drugs: Action of β1 Blockers

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, β1-blockers...
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

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

Antihypertensive Drugs: Angiotensin II Receptor Blockers

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...
Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

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,...
Antihypertensive Drugs: Vasodilators01:23

Antihypertensive Drugs: Vasodilators

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...
Hypertension II: Pathophysiology01:29

Hypertension II: Pathophysiology

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,...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Regression of gastric de novo diffuse large B-cell lymphoma following Helicobacter pylori eradication: a case report.

Acta gastro-enterologica Belgica·2016
Same author

Elastic cartilage reconstruction by transplantation of cultured hyaline cartilage-derived chondrocytes.

Transplantation proceedings·2014
Same author

A randomized phase III trial of postoperative adjuvant therapy for completely resected stage IA-IIIA lung cancer using an anti‑angiogenetic agent: irsogladine maleate.

Minerva chirurgica·2013
Same author

PARG dysfunction enhances DNA double strand break formation in S-phase after alkylation DNA damage and augments different cell death pathways.

Cell death & disease·2013
Same author

Poly(ADP-ribose) Glycohydrolase deficiency sensitizes mouse ES cells to DNA damaging agents.

Current cancer drug targets·2009
Same author

Widely tunable 90 degree phase-matched KTP parametric oscillator.

Optics letters·2009

Related Experiment Video

Updated: Jul 22, 2026

Mesenteric Artery Contraction and Relaxation Studies Using Automated Wire Myography
07:51

Mesenteric Artery Contraction and Relaxation Studies Using Automated Wire Myography

Published on: September 22, 2011

A decrease in the amount and function of inhibitory GTP-binding protein in the resistance small artery from

M Masutani1, M Ohyanagi, J Shibuya

  • 1First Department of Internal Medicine, Hyogo College of Medicine, Nishinomiya, Japan.

Japanese Journal of Pharmacology
|April 15, 1999
PubMed
Summary

The inhibitory GTP-binding protein (Gi protein) declines in peripheral arteries of spontaneously hypertensive rats before hypertension onset. This suggests a role for Gi protein dysfunction in hypertension development.

More Related Videos

Assessing Myogenic Response and Vasoactivity In Resistance Mesenteric Arteries Using Pressure Myography
10:48

Assessing Myogenic Response and Vasoactivity In Resistance Mesenteric Arteries Using Pressure Myography

Published on: July 6, 2015

Evaluation of Vascular Control Mechanisms Utilizing Video Microscopy of Isolated Resistance Arteries of Rats
10:28

Evaluation of Vascular Control Mechanisms Utilizing Video Microscopy of Isolated Resistance Arteries of Rats

Published on: December 5, 2017

Related Experiment Videos

Last Updated: Jul 22, 2026

Mesenteric Artery Contraction and Relaxation Studies Using Automated Wire Myography
07:51

Mesenteric Artery Contraction and Relaxation Studies Using Automated Wire Myography

Published on: September 22, 2011

Assessing Myogenic Response and Vasoactivity In Resistance Mesenteric Arteries Using Pressure Myography
10:48

Assessing Myogenic Response and Vasoactivity In Resistance Mesenteric Arteries Using Pressure Myography

Published on: July 6, 2015

Evaluation of Vascular Control Mechanisms Utilizing Video Microscopy of Isolated Resistance Arteries of Rats
10:28

Evaluation of Vascular Control Mechanisms Utilizing Video Microscopy of Isolated Resistance Arteries of Rats

Published on: December 5, 2017

Area of Science:

  • Cardiovascular Physiology
  • Molecular Biology
  • Hypertension Research

Background:

  • The inhibitory GTP-binding protein (Gi protein) is crucial for vascular tone regulation, particularly in conduit vessels.
  • Its specific role in peripheral microvascular tone control during hypertension remains unclear.
  • Understanding Gi protein's function in hypertension is vital for developing targeted therapies.

Purpose of the Study:

  • To investigate Gi protein concentration and function in peripheral resistance arteries and aorta of hypertensive rats.
  • To determine if Gi protein alterations precede hypertension onset in spontaneously hypertensive rats (SHR).
  • To compare these changes with secondary hypertension models (renovascular hypertensive rats, RHR).

Main Methods:

  • Immunohistochemistry was used to semiquantitatively assess Gi protein alpha2 subunit concentration in rat aorta and cremaster small arteries.
  • Microcannulation techniques evaluated Gi protein function in relation to alpha2-adrenoceptor.
  • Studies included spontaneously hypertensive rats (SHR), normotensive Wistar-Kyoto rats (WKY), and renovascular hypertensive rats (RHR).

Main Results:

  • A significant reduction in Gi protein alpha2 subunits was observed in the cremaster small artery of SHR from 4 weeks of age compared to WKY.
  • Gi protein function related to alpha2-adrenoceptor was diminished in SHR even before the onset of hypertension.
  • No significant differences in Gi protein levels were found between RHR and WKY.

Conclusions:

  • A quantitative and functional decline in Gi protein occurs in peripheral small artery smooth muscle cells of SHR prior to hypertension development.
  • This finding suggests that Gi protein dysfunction may contribute to the pathogenesis of spontaneous hypertension.
  • Secondary hypertension models (RHR) did not exhibit these pre-hypertensive Gi protein changes.