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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: 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,...
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,...
Acute Kidney Injury II: Pathophysiology01:29

Acute Kidney Injury II: Pathophysiology

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Updated: May 25, 2026

Single-channel Analysis and Calcium Imaging in the Podocytes of the Freshly Isolated Glomeruli
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Published on: June 27, 2015

Angiotensin II, a missing node in new pathogenic glomerulotubular feedback loop.

Jian-Dong Zhang1, Bi-Cheng Liu

  • 1Institute of Nephrology, Zhongda Hospital, Southeast University, Nanjing 210009, China.

Medical Hypotheses
|July 26, 2011
PubMed
Summary
This summary is machine-generated.

This study introduces Angiotensin II (Ang II) into the proposed kidney feedback loop, identifying its interaction with immune cells. Understanding this mechanism may prevent acute kidney diseases from becoming chronic.

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Area of Science:

  • Nephrology
  • Immunology
  • Cardiovascular Research

Background:

  • A pathogenic glomerulotubular feedback loop is implicated in acute kidney disease progression to chronic status.
  • Immune cells are central to this proposed feedback loop.
  • Existing models have limitations in explaining the transition to chronic kidney disease.

Purpose of the Study:

  • To amend the existing glomerulotubular feedback loop model.
  • To investigate the role of Angiotensin II (Ang II) in acute-to-chronic kidney disease transition.
  • To explore the interaction between Ang II and immune cells within this context.

Main Methods:

  • Conceptual amendment of the feedback loop paradigm.
  • Review and integration of existing literature on kidney disease pathways.
  • Hypothetical modeling of Ang II and immune cell interactions.

Main Results:

  • Angiotensin II (Ang II) is proposed as a critical, previously missing component of the feedback loop.
  • The interaction between Ang II and immune cells is highlighted as a key factor.
  • The amended model provides a more comprehensive view of acute-to-chronic kidney disease transition.

Conclusions:

  • The inclusion of Ang II refines the understanding of the glomerulotubular feedback loop.
  • Investigating Ang II and immune cell interplay offers potential therapeutic targets.
  • This research may lead to novel strategies for preventing acute kidney disease chronicity.