Skip to content
2000
  • ISSN: 1568-0142
  • E-ISSN: 1875-6131

Abstract

Nitric oxide is a key player among the numerous mediators of endothelial homeostasis and cardiac contractility and is thereby involved in the pathogenic processes leading to vascular and myocardial dysfunctions. Although none of the current paradigms would elevate the influence of NO on cardiac contraction to the level of that of e.g., catecholamines or increased calcium, this unusual signaling molecule can modulate virtually all the regulatory steps of excitationcontraction coupling and influence the course of cardiac decompensation. Not only alterations in spatial confinement or post-translational modifications but also changes in the abundance of one of the three NOS isoforms may result in profound cellular disturbancies that participate in the endothelial and contractile dysfunctions leading to cardiovascular diseases.

Loading

Article metrics loading...

/content/journals/cmcaiaa/10.2174/1568014043355348
2004-09-01
2025-09-21
Loading full text...

Full text loading...

/content/journals/cmcaiaa/10.2174/1568014043355348
Loading
This is a required field
Please enter a valid email address
Approval was a Success
Invalid data
An Error Occurred
Approval was partially successful, following selected items could not be processed due to error
Please enter a valid_number test