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Related Concept Videos

Hormonal Regulation01:33

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.
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: 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...
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,...
Hormonal Regulation of Blood Pressure01:17

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...

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Related Experiment Video

Updated: Jun 1, 2026

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors
12:03

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors

Published on: June 7, 2016

The renin-angiotensin system.

Kar Neng Lai, Joseph C K Leung, Sydney C W Tang

    Contributions to Nephrology
    |June 11, 2011
    PubMed
    Summary
    This summary is machine-generated.

    Diabetic nephropathy involves kidney damage mediated by the renin-angiotensin system (RAS). Understanding intraglomerular RAS in hyperglycemia offers new approaches for early diabetic kidney disease detection and treatment.

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    Last Updated: Jun 1, 2026

    Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors
    12:03

    Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors

    Published on: June 7, 2016

    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

    Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion
    08:35

    Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion

    Published on: May 26, 2022

    Area of Science:

    • Nephrology
    • Endocrinology
    • Molecular Biology

    Background:

    • Diabetic nephropathy (DN) is a major cause of end-stage renal disease, driven by type 2 diabetes.
    • The renin-angiotensin system (RAS), particularly Angiotensin II (Ang II), is a key mediator of renal injury in DN.
    • Hyperglycemia and mechanical stress from glomerular hypertension are critical factors in DN pathogenesis.

    Purpose of the Study:

    • To investigate the role of the intraglomerular RAS in diabetic nephropathy.
    • To explore how hyperglycemia alters podocyte function and RAS balance.
    • To identify novel approaches for early DN intervention.

    Main Methods:

    • Review of existing literature on DN pathogenesis and RAS.
    • Analysis of signaling pathways affected by hyperglycemia and mechanical stress.
    • Examination of podocyte's role in maintaining intraglomerular RAS homeostasis.

    Main Results:

    • Ang II promotes inflammation and fibrosis in DN by upregulating chemokines and growth factors.
    • High glucose and mechanical stress synergistically damage podocytes, impairing their structural integrity.
    • Podocyte's normal RAS-balancing enzymatic activities are disrupted in hyperglycemic conditions.

    Conclusions:

    • Podocyte injury is an early event in DN, leading to irreversible renal damage.
    • Altered intraglomerular RAS activity in hyperglycemia contributes significantly to DN progression.
    • Targeting the local RAS offers a promising strategy for managing early-stage diabetic nephropathy.