Related Experiment Video

Updated: May 22, 2026

Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion
08:35

Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion

Published on: May 26, 2022

Chlorella pyrenoidosa ameliorated L-NAME-induced hypertension and cardiorenal remodeling in rats

Su-Ching Yang1, Hsin-Yi Yang, Yi-Ching Yang

  • 1School of Nutrition and Health Sciences, Taipei Medical University, Taipei, Taiwan.

European Journal of Nutrition
|May 4, 2012
PubMed

Insights

Chlorella pyrenoidosa supplementation effectively lowered blood pressure and protected against cardiorenal damage in hypertensive rats. This natural intervention may offer a therapeutic strategy for cardiovascular health by inhibiting ACE activity.

Area of Science:

  • Cardiovascular Science
  • Nutritional Science
  • Pharmacology

Background:

  • Hypertension is a primary risk factor for cardiovascular diseases.
  • Endothelial dysfunction, induced by N (ω)-nitro-L-arginine methyl ester hydrochloride (L-NAME), serves as a model for studying hypertension.
  • Cardiorenal remodeling is a significant pathological consequence of sustained hypertension.

Purpose of the Study:

  • To evaluate the impact of Chlorella pyrenoidosa on blood pressure in L-NAME-induced hypertensive rats.
  • To assess the effects of Chlorella pyrenoidosa on cardiorenal remodeling.
  • To explore potential mechanisms underlying Chlorella pyrenoidosa's effects, including ACE inhibition.

Main Methods:

  • Rats were administered L-NAME (40 mg/kg) with or without Chlorella pyrenoidosa (4% or 8%) in their diet for 5 weeks.
  • Blood pressure and cardiorenal parameters were monitored throughout the experimental period.
  • Plasma and tissue samples were analyzed for ACE activity, nitric oxide metabolites, arginine, tumor necrosis factor-α, and CYP4A expression.

Main Results:

  • Chlorella pyrenoidosa supplementation significantly attenuated the development of hypertension and cardiorenal remodeling.
  • ACE activity in plasma and tissues was notably reduced in rats treated with Chlorella pyrenoidosa.
  • Levels of tumor necrosis factor-α and renal CYP4A expression were decreased in the Chlorella pyrenoidosa groups.

Conclusions:

  • Chlorella pyrenoidosa demonstrates cardiorenal protective effects in a rat model of nitric oxide deficiency.
  • The antihypertensive and cardiorenal protective effects of Chlorella pyrenoidosa may be attributed to its angiotensin-converting enzyme (ACE) inhibitory activity.
  • These findings suggest Chlorella pyrenoidosa as a potential therapeutic agent for managing hypertension and related cardiovascular complications.
Abstract

More Related Videos

5/6th Nephrectomy in Combination with High Salt Diet and Nitric Oxide Synthase Inhibition to Induce Chronic Kidney Disease in the Lewis Rat08:50

5/6th Nephrectomy in Combination with High Salt Diet and Nitric Oxide Synthase Inhibition to Induce Chronic Kidney Disease in the Lewis Rat

Published on: July 3, 2013

A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats07:31

A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats

Published on: December 2, 2016

Related Concept Videos

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...
Heart Failure Drugs: Diuretics01:22

Heart Failure Drugs: Diuretics

Heart failure and kidney perfusion are interconnected in a complex way. Reduced renal perfusion and venous congestion are two significant factors that contribute to renal dysfunction in heart failure. The kidneys, primarily responsible for fluid balance in the body, are adversely affected due to compromised cardiac output and increased venous pressure. In response to reduced renal perfusion, the kidneys activate neurohumoral mechanisms to restore balance. However, these mechanisms can be...
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...
Cardiomyopathy V: Interprofessional Care01:29

Cardiomyopathy V: Interprofessional Care

Managing cardiomyopathy involves addressing underlying or precipitating causes, treating heart failure with medications, and implementing dietary changes and a balanced exercise and rest regimen.Lifestyle ModificationsCardiomyopathy patients should adopt a low-sodium diet to reduce fluid retention and manage heart failure. A personalized exercise and rest plan helps maintain physical fitness without overstraining the heart. Avoiding alcohol and tobacco is essential to prevent further damage to...
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,...