Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Hormonal Regulation

Hormonal Regulation

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.

Hormonal Regulation of Blood Pressure

Hormonal Regulation of Blood Pressure

Endocrinal or hormonal intervention in the cardiovascular system is predominantly exerted by the catecholamines - epinephrine and norepinephrine, as well as a slew of hormones that interact with renal function to modulate blood volume.
Epinephrine and Norepinephrine
The adrenal medulla releases epinephrine and norepinephrine, catecholamines that enhance and extend the sympathetic or "fight or flight" physiological response. These hormones escalate heart rate and the force of contraction while...

Antihypertensive Drugs: Angiotensin II Receptor Blockers

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...

Introduction to Urinary System

Introduction to Urinary System

The urinary system consists of two kidneys, two ureters, the urinary bladder, and the urethra.
The kidneys are bean-shaped organs located in the retroperitoneal space, on either side of the vertebral column, between the T12 and L3 vertebrae. They are partially protected by the rib cage and surrounded by perirenal fat, which provides cushioning. They are responsible for urine formation and play critical roles in regulating blood pressure, electrolyte levels, and hormone production. The ureters...

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

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: Potassium-Sparing Diuretics

Antihypertensive Drugs: Potassium-Sparing Diuretics

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...

You might also read

Related Articles

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

Sort by

Same author

Exercise volume modulates cardiac protection in a type 2 diabetic rat model: differential effects of high- and low-volume moderate-intensity endurance exercise training on diabetic cardiomyopathy.

Cardiovascular diabetology. Endocrinology reports·2026

Same author

Mitochondrial Transplantation as a New Therapeutic Approach Against Cardiac and Renal Consequences in Male Rats With Myocardial Infarction.

Acta physiologica (Oxford, England)·2026

Same author

Clinical Improvements Following a Non-Aerobic Therapeutic Exercise in Women with Long COVID.

Journal of clinical medicine·2025

Same author

From Likes to Learning: How Social Media and Memes Can Transform Nursing Education.

Computers, informatics, nursing : CIN·2025

Same author

What about applied kinanthropometry in wheelchair basketball? Proposal for anthropometric references in Spanish elite players.

Sports medicine - open·2025

Same author

A comparison of cryopreserved and noncryopreserved peripheral blood hematopoietic stem cells for autologous transplantation in multiple myeloma: a study from the chronic malignancies working party of the EBMT.

Cytotherapy·2025

Search research articles

Related Experiment Video

Updated: Jul 6, 2026

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors

Published on: June 7, 2016

Aldosterone and the vascular system.

Victoria Cachofeiro¹, Maria Miana, Natalia de Las Heras

¹Department of Physiology, School of Medicine, Universidad Complutense, Madrid, Spain. vcara@med.ucm.es

The Journal of Steroid Biochemistry and Molecular Biology

|April 11, 2008

Summary

Aldosterone contributes to vascular damage in hypertension by impairing endothelial function and promoting inflammation and remodeling. Blocking its mineralocorticoid receptor can improve vascular health.

More Related Videos

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

Published on: September 26, 2018

Isolation and Adoptive Transfer of High Salt Treated Antigen-presenting Dendritic Cells

Isolation and Adoptive Transfer of High Salt Treated Antigen-presenting Dendritic Cells

Published on: March 5, 2019

Related Experiment Videos

Last Updated: Jul 6, 2026

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors

Published on: June 7, 2016

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

Published on: September 26, 2018

Isolation and Adoptive Transfer of High Salt Treated Antigen-presenting Dendritic Cells

Isolation and Adoptive Transfer of High Salt Treated Antigen-presenting Dendritic Cells

Published on: March 5, 2019

Area of Science:

Cardiovascular biology
Endocrinology
Vascular medicine

Background:

Aldosterone exerts diverse physiological and pathological effects across various tissues.
Vascular effects of aldosterone include impaired endothelial function and contribution to pathologies like hypertension and atherosclerosis.

Purpose of the Study:

To elucidate the mechanisms by which aldosterone contributes to vascular damage.
To investigate the role of aldosterone in endothelial dysfunction, inflammation, and vascular remodeling.

Main Methods:

Administration of aldosterone and mineralocorticoid receptor antagonists (e.g., eplerenone).
Assessment of endothelium-dependent relaxations and nitric oxide levels.
Evaluation of inflammatory markers (NF-kappaB activation, cytokine production) and vascular remodeling (media-to-lumen ratio).

Main Results:

Aldosterone impaired endothelium-dependent relaxations, linked to reduced nitric oxide production and increased degradation by reactive oxygen species.
Aldosterone promoted vascular inflammation via NF-kappaB activation and cytokine production.
Mineralocorticoid receptor antagonism improved vascular remodeling in hypertensive rats.

Conclusions:

Aldosterone promotes vascular damage through pro-oxidant, pro-inflammatory, and profibrotic effects mediated by mineralocorticoid receptors.
These effects contribute to endothelial dysfunction, inflammation, and vascular remodeling in conditions like hypertension.
Targeting the mineralocorticoid receptor may offer therapeutic benefits for vascular pathologies.