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Related Concept Videos

Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

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...
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...
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

Acute kidney injury (AKI) causes are categorized into three primary categories based on the location of the injury: prerenal, intrarenal (or intrinsic), and postrenal causes. This classification guides clinical management and illustrates how different pathways can impair kidney function.Etiology and Pathophysiology of Acute Kidney Injury1. Prerenal causesEtiology: Prerenal Acute Kidney Injury, the most common type, occurs when reduced blood flow to the kidneys decreases filtration capacity...
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

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...
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,...

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Related Experiment Video

Updated: Jun 18, 2026

Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice
07:21

Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice

Published on: September 28, 2015

Angiotensin II in experimental hyperdynamic sepsis.

Li Wan1, Christoph Langenberg, Rinaldo Bellomo

  • 1Howard Florey Institute, University of Melbourne, Parkville, Melbourne, Victoria 3052, Australia. li.wan@austin.org.au

Critical Care (London, England)
|December 2, 2009
PubMed
Summary

Angiotensin II (Ang II) infusion improved kidney function in early sepsis, increasing urine output and normalizing creatinine clearance despite reduced renal blood flow. This vasopressor shows promise for treating hypotensive hyperdynamic sepsis.

Related Experiment Videos

Last Updated: Jun 18, 2026

Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice
07:21

Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice

Published on: September 28, 2015

Area of Science:

  • Critical care medicine
  • Cardiovascular physiology
  • Renal medicine

Background:

  • Sepsis-induced hypotension requires vasopressor support.
  • Angiotensin II (Ang II) is a potential vasopressor for sepsis.
  • Its effects on regional blood flow and renal function in sepsis are unknown.

Purpose of the Study:

  • To investigate the systemic, regional blood flow, and renal functional effects of Ang II in experimental hypotensive hyperdynamic sepsis.

Main Methods:

  • Conscious ewes underwent instrumentation with arterial flow probes.
  • Hyperdynamic sepsis was induced via intravenous E. coli administration.
  • Animals received either placebo or titrated Ang II infusion to maintain baseline blood pressure.

Main Results:

  • Sepsis increased renal blood flow but caused oliguria and decreased creatinine clearance.
  • Ang II restored arterial pressure but reduced renal blood flow compared to placebo.
  • Despite reduced renal blood flow, Ang II significantly increased urine output and normalized creatinine clearance.

Conclusions:

  • Intravenous Ang II infusion in early experimental sepsis improved renal function.
  • Ang II increased urine output and normalized creatinine clearance.
  • Ang II did not significantly affect other regional blood flows.