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Related Concept Videos

Hypertension II: Pathophysiology01:29

Hypertension II: Pathophysiology

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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,...
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Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

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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,...
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Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

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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...
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Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

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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...
2.1K
Hormonal Regulation01:33

Hormonal Regulation

35.3K
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.
35.3K
Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

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Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
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Updated: Dec 15, 2025

A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis
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COVID-19, Renin-Angiotensin System and Endothelial Dysfunction.

Razie Amraei1, Nader Rahimi1

  • 1Department of Pathology, School of Medicine, Boston University Medical Campus, Boston, MA 02118, USA.

Cells
|July 15, 2020
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The SARS-CoV-2 virus enters cells via ACE2, disrupting the renin-angiotensin system and causing vascular damage. This review explores COVID-19

Keywords:
ACE2CD209LL-SIGNSARS-CoV-2endothelial cell injuryendothelial dysfunction

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Last Updated: Dec 15, 2025

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Area of Science:

  • Cardiovascular Biology
  • Virology
  • Immunology

Background:

  • The COVID-19 pandemic, caused by SARS-CoV-2, poses a significant global health threat.
  • Angiotensin-converting enzyme 2 (ACE2) is crucial for SARS-CoV-2 entry and plays a key role in cardiovascular homeostasis via the renin-angiotensin system (RAS).
  • Endothelial dysfunction, common in aging and chronic diseases, may worsen SARS-CoV-2-induced vascular injury.

Purpose of the Study:

  • To review the molecular mechanisms of SARS-CoV-2 infection.
  • To elucidate the roles of ACE2 and RAS signaling in COVID-19 pathogenesis.
  • To explore the link between pre-existing endothelial dysfunction and COVID-19 mortality.

Main Methods:

  • Literature review of molecular mechanisms of SARS-CoV-2 infection.
  • Analysis of the role of ACE2 and RAS in viral entry and pathogenesis.
  • Survey of cell adhesion molecules (CAMs) in viral infections.

Main Results:

  • SARS-CoV-2 utilizes ACE2 for cell entry, leading to ARDS, cytokine storms, and vascular damage.
  • ACE2 activity is vital for regulating cardiovascular homeostasis through RAS.
  • Endothelial cell injury by SARS-CoV-2 can exacerbate pre-existing endothelial dysfunction, contributing to mortality.

Conclusions:

  • Understanding SARS-CoV-2's molecular basis and vascular effects is key to developing treatments.
  • Targeting ACE2, RAS, and endothelial dysfunction pathways may offer therapeutic strategies for COVID-19.
  • Investigating CAMs like CD209L/L-SIGN and CD209/DC-SIGN may reveal insights into viral infection.