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Related Experiment Video

Updated: May 18, 2026

Continuous IV Infusion is the Choice Treatment Route for Arginine-vasopressin Receptor Blocker Conivaptan in Mice to Study Stroke-evoked Brain Edema

Continuous IV Infusion is the Choice Treatment Route for Arginine-vasopressin Receptor Blocker Conivaptan in Mice to Study Stroke-evoked Brain Edema

Published on: September 1, 2016

Tolvaptan improves left ventricular dysfunction after myocardial infarction in rats.

Takanori Yamazaki¹, Yasukatsu Izumi, Yasuhiro Nakamura

¹Department of Internal Medicine and Cardiology, Osaka City University Medical School, Osaka, Japan.

Circulation. Heart Failure

|September 18, 2012

Summary

Tolvaptan improved cardiac function in rats with heart failure after myocardial infarction (MI). This novel drug reduced cardiac volumes and fibrosis, offering a potential new treatment for heart failure.

More Related Videos

Acute Myocardial Infarction in Rats

Acute Myocardial Infarction in Rats

Published on: February 16, 2011

Related Experiment Videos

Last Updated: May 18, 2026

Continuous IV Infusion is the Choice Treatment Route for Arginine-vasopressin Receptor Blocker Conivaptan in Mice to Study Stroke-evoked Brain Edema

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Published on: September 1, 2016

Acute Myocardial Infarction in Rats

Acute Myocardial Infarction in Rats

Published on: February 16, 2011

Area of Science:

Cardiology
Pharmacology

Background:

Arginine vasopressin levels increase in chronic heart failure, contributing to renal water reabsorption.
Left ventricular dysfunction following myocardial infarction (MI) is a significant clinical challenge.

Purpose of the Study:

To compare the efficacy of tolvaptan, a V(2) receptor antagonist, with furosemide and a combination therapy in a rat model of post-MI left ventricular dysfunction.
To investigate the impact of tolvaptan on cardiac remodeling, inflammation, and neurohumoral activation.

Main Methods:

Rats with established MI were randomized into groups receiving vehicle, furosemide, tolvaptan (3 or 10 mg·kg(-1)·day(-1)), or furosemide plus tolvaptan for 4 weeks.
Cardiac volumes, ejection fraction, macrophage infiltration, interstitial fibrosis, and gene expression of key cardiac markers were assessed.

Main Results:

Tolvaptan treatment significantly reduced left ventricular end-diastolic and systolic volumes and improved ejection fraction compared to vehicle.
Tolvaptan suppressed MI-induced macrophage infiltration and interstitial fibrosis in the left ventricle.
Tolvaptan attenuated the expression of genes associated with neurohumoral activation (natriuretic peptides, vasopressin V(1a) receptor, endothelin-1) and inflammation (monocyte chemotactic protein-1).

Conclusions:

Tolvaptan demonstrates potential in improving cardiac dysfunction post-MI.
The beneficial effects of tolvaptan may be attributed to the suppression of the vasopressin V(1a) receptor, neurohumoral pathways, and inflammatory processes.