Nitric oxide and cardiac failure

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Updated: Oct 31, 2026

Chemiluminescence-based Assays for Detection of Nitric Oxide and its Derivatives from Autoxidation and Nitrosated Compounds
08:23

Chemiluminescence-based Assays for Detection of Nitric Oxide and its Derivatives from Autoxidation and Nitrosated Compounds

Published on: February 16, 2022

U Ikeda1, K Shimada

  • 1Department of Cardiology, Jichi Medical School, Tochigi, Japan.

Clinical Cardiology
|October 23, 1997
PubMed

Insights

Cardiac myocytes produce nitric oxide (NO) via eNOS and iNOS. Increased inducible NO synthase (iNOS) in heart failure contributes to cardiac dysfunction and cell damage.

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Biomedical Science

Background:

  • Cardiac myocytes express two nitric oxide (NO) synthase isoforms: endothelial NO synthase (eNOS) and inducible NO synthase (iNOS).
  • eNOS activity is modulated by cardiac contractility, whereas iNOS expression is induced by inflammatory cytokines.
  • Cytokine-induced NO production negatively impacts cardiac myocyte function and viability.

Purpose of the Study:

  • To investigate the role and implications of iNOS expression in cardiac myocytes, particularly in the context of heart failure.
  • To understand the relationship between neurohumoral factors, iNOS expression, and cardiac dysfunction in chronic heart failure.

Main Methods:

  • Analysis of iNOS expression in cardiac myocytes.
  • Investigation of iNOS regulation by cytokines and neurohumoral factors.
  • Assessment of the functional and viability effects of NO produced by iNOS.

Main Results:

  • iNOS expression is elevated in the myocardium of patients with dilated cardiomyopathy and heart failure.
  • Activated neurohumoral factors in chronic heart failure exacerbate cardiac iNOS expression.
  • Elevated iNOS activity contributes to cardiac dysfunction and myocyte damage.

Conclusions:

  • Increased cardiac iNOS expression is a significant factor in the pathophysiology of heart failure.
  • Targeting iNOS may offer a therapeutic strategy for managing heart failure and preventing cardiac damage.

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