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Related Concept Videos

Antihypertensive Drugs: Direct Renin Inhibitors01:25

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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

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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

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

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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...
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Heart Failure V: Medical Management01:30

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Medical Management of Acute Decompensated Heart Failure (ADHF)The primary goals of therapy for patients hospitalized with acute decompensated heart failure (ADHF) include:Relieving symptomsOptimizing volume statusSupporting oxygenation and ventilationMaintaining cardiac output (CO) and end-organ perfusionIdentifying and addressing the cause of ADHFPreventing complicationsProviding patient education on factors precipitating HF exacerbationPlanning for dischargeOngoing monitoring and assessment...
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Hormonal Regulation01:33

Hormonal Regulation

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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.
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Renin-Angiotensin System Inhibitors in COVID-19: Current Concepts.

Kunal Mahajan1, Prakash Chand Negi1, Neeraj Ganju1

  • 1Department of Cardiology, Indira Gandhi Medical College, Shimla 171001, India.

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The safety of renin-angiotensin system (RAS) inhibitors for COVID-19 patients remains unclear. While some studies suggest potential harm, others propose protective effects, necessitating further research.

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Area of Science:

  • Cardiovascular Medicine
  • Infectious Diseases
  • Pharmacology

Background:

  • The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) uses angiotensin-converting enzyme-2 (ACE-2) as its functional receptor.
  • ACE-2 plays a crucial role in regulating the renin-angiotensin system (RAS).

Purpose of the Study:

  • To review current data and pathophysiological mechanisms concerning the interaction between RAS inhibitors and COVID-19.
  • To address the conflicting hypotheses regarding the safety and efficacy of RAS inhibitors in COVID-19 patients.

Main Methods:

  • Literature review of preclinical studies and existing data on RAS inhibitors and COVID-19.
  • Analysis of the pathophysiological interplay between the renin-angiotensin system, ACE-2, and SARS-CoV-2 infection.

Main Results:

  • Preclinical studies show RAS inhibitors can increase ACE-2 expression, raising concerns about facilitating viral entry.
  • Conversely, some hypotheses suggest RAS inhibitors might offer protection against COVID-19-related lung injury.

Conclusions:

  • Current data are insufficient to definitively conclude the safety or efficacy of RAS inhibitors in COVID-19 patients.
  • Human trials are critically needed to evaluate the effects of RAS inhibitors in the context of COVID-19.