Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

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: Diuretics

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...

Heart Failure II: Pathophysiology

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...

Heart Failure Drugs: β-Blockers

Heart Failure Drugs: β-Blockers

β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation, vasodilation, and...

Antihypertensive Drugs: Direct Renin Inhibitors

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,...

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Hepatic chemosaturation with melphalan in patients with primary or secondary liver tumors with or without extrahepatic tumor manifestation.

ESMO gastrointestinal oncology·2026

Same author

Tibetans exhibit lower hemoglobin concentration and decreased heart response to hypoxia during poikilocapnia at intermediate altitude relative to Han Chinese.

Frontiers in physiology·2024

Same author

Where Does Some of the Ingested Sodium Chloride Hide without Exerting Osmotic Pressure?: Internal Sodium Balance in DOCA-Salt Rats: A Body Composition Study. Am J Renal Physiol 289: F793-F802, 2005.

Journal of the American Society of Nephrology : JASN·2023

Same author

Renal replacement therapy-requiring acute kidney injury due to tubulointerstitial nephritis and uveitis syndrome: case report.

Journal of medical case reports·2021

Same author

Hemophagocytic lymphohistiocytosis and thrombotic microangiopathy after parvovirus B19 infection and renal transplantation: a case report.

BMC nephrology·2021

Same author

COVID-19 effects on the kidney.

Der Pathologe·2021

Same journal

Blood Pressure Responses to Dietary Salt in Renin-Deficient Dahl Salt-Sensitive Rats.

American journal of physiology. Renal physiology·2026

Same journal

Cytokine Profiles in Patients with Chronic Kidney Disease and Low Sexual Function.

American journal of physiology. Renal physiology·2026

Same journal

Renovascular disease induces functionally relevant, locus-specific alterations to DNA methylation and hydroxymethylation in swine scattered tubular-like cells.

American journal of physiology. Renal physiology·2026

Same journal

Nitrite Protects Against Cardiac Surgery-Associated Acute Kidney Injury via Inflammation Suppression: Insights from a Rat Cardiopulmonary Bypass Model.

American journal of physiology. Renal physiology·2026

Same journal

Etanercept attenuates TNFα-mediated kidney injury in a rat model of brain death kidney donation.

American journal of physiology. Renal physiology·2026

Same journal

Phosphorylation of aquaporin-2 at serine 269 in urinary extracellular vesicles reflects renal vasopressin activity in rats.

American journal of physiology. Renal physiology·2026

See all related articles

Search research articles

Related Experiment Video

Updated: Jun 7, 2026

Intravascular Delivery of Biologics to the Rat Kidney

Intravascular Delivery of Biologics to the Rat Kidney

Published on: September 1, 2016

Sympathetic blockade prevents the decrease in cardiac VEGF expression and capillary supply in experimental renal

K Amann¹, G Odoni, K Benz

¹Department of Pathology, University of Erlangen-Nürnberg, Krankenhausstr. 8-10, 91054 Erlangen, Germany. kerstin.amann@uk-erlangen.de

American Journal of Physiology. Renal Physiology

|October 22, 2010

Summary

This summary is machine-generated.

Kidney failure reduces cardiac vascular endothelial growth factor (VEGF) in rats, impairing heart function. Blocking the sympathetic nervous system may improve cardiac VEGF levels and heart health.

More Related Videos

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

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

Published on: October 26, 2020

Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion

Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion

Published on: May 26, 2022

Related Experiment Videos

Last Updated: Jun 7, 2026

Intravascular Delivery of Biologics to the Rat Kidney

Intravascular Delivery of Biologics to the Rat Kidney

Published on: September 1, 2016

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

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

Published on: October 26, 2020

Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion

Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion

Published on: May 26, 2022

Area of Science:

Cardiovascular research
Renal disease mechanisms
Molecular biology

Background:

Uremic cardiomyopathy is linked to reduced myocardial capillary supply.
Sympathetic nervous system blockade can prevent cardiac issues in uremic rats.
The role of vascular endothelial growth factor (VEGF) in uremic cardiomyopathy is unclear.

Purpose of the Study:

To investigate if cardiac vascular endothelial growth factor (VEGF) gene and protein expression are altered in experimental renal failure.
To determine the effect of sympathetic nervous system downregulation on cardiac VEGF expression and myocardial capillary supply in rats with renal failure.

Main Methods:

Long-term study: Compared VEGF gene and protein expression and capillary supply in Sprague-Dawley rats with subtotal nephrectomy (SNX) versus sham operation.
Short-term study: Analyzed the effect of renal denervation on cardiac VEGF, flt-1, and flk-1 gene expression and myocardial capillary supply in SNX rats.

Main Results:

Long-term: SNX rats showed significantly lower cardiac capillary supply and VEGF gene/protein expression compared to sham rats.
Short-term: Untreated SNX rats had significantly lower cardiac VEGF mRNA expression than sham rats.
Renal denervation prevented the decrease in cardiac VEGF mRNA expression in SNX rats.

Conclusions:

Cardiac VEGF gene and protein expression are reduced in experimental renal failure.
Reduced cardiac VEGF may contribute to impaired myocardial adaptation and hypertrophy in renal failure.
Sympathetic nervous system downregulation may improve cardiac structure and function in renal failure partly via increased cardiac VEGF expression.