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Related Concept Videos

Hormonal Regulation01:33

Hormonal Regulation

33.6K
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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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...
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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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Hormonal Regulation of Blood Pressure01:17

Hormonal Regulation of Blood Pressure

3.1K
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...
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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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Related Experiment Video

Updated: Sep 2, 2025

Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice
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Angiotensin 1-7 and its analogue decrease blood pressure but aggravate renal damage in preeclamptic mice.

Yuan Liu1, Ruonan Zhai1, Jiahao Tong1

  • 1Department of Nephrology, Shanghai Fifth People's Hospital, Fudan University, 801 Heqing Road, Shanghai 200240, P.R. China.

Experimental Animals
|August 7, 2022
PubMed
Summary

Agonistic autoantibodies to the angiotensin II type I receptor (AT1-AA) cause preeclampsia (PE) symptoms. Angiotensin 1-7 (Ang 1-7) and AVE0991 lowered blood pressure in a PE mouse model but worsened kidney damage.

Keywords:
agonistic autoantibodies to the angiotensin II type I receptorangiotensin 1-7animal modelpreeclampsiarenal damage

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A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis
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Area of Science:

  • Reproductive medicine
  • Nephrology
  • Cardiovascular research

Background:

  • Preeclampsia (PE) is a serious pregnancy complication impacting maternal and fetal health.
  • Agonistic autoantibodies to the angiotensin II type I receptor (AT1-AA) are implicated in PE pathogenesis.

Purpose of the Study:

  • To investigate the effects of Angiotensin 1-7 (Ang 1-7) and its analogue AVE0991 on an AT1-AA-induced preeclampsia mouse model.
  • To evaluate the therapeutic potential of Ang 1-7 and AVE0991 in managing PE-related hypertension and renal dysfunction.

Main Methods:

  • An AT1-AA-induced preeclampsia mouse model was established on gestational day 13.
  • Mice were treated with vehicle, Losartan, Ang 1-7, or AVE0991.
  • Systolic blood pressure, proteinuria, blood urea nitrogen, and renal histology were assessed.

Main Results:

  • The AT1-AA-induced PE model exhibited elevated blood pressure and proteinuria, characteristic of PE.
  • Treatment with Ang 1-7 or AVE0991 significantly reduced systolic blood pressure in the PE mice.
  • Neither Ang 1-7 nor AVE0991 demonstrated renoprotective effects; instead, they aggravated renal damage.

Conclusions:

  • Ang 1-7 and its analogue AVE0991 effectively lower blood pressure in an AT1-AA-induced preeclampsia mouse model.
  • Despite antihypertensive effects, Ang 1-7 and AVE0991 exacerbate renal damage in this PE model, suggesting potential risks.
  • Further research is needed to understand the complex role of the Ang 1-7 pathway in preeclampsia and its impact on renal health.