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Nitric oxide attenuates cardiac myocyte contraction
A J Brady1, J B Warren, P A Poole-Wilson
1Department of Cardiac Medicine, National Heart and Lung Institute, London, United Kingdom.
The American Journal of Physiology
|July 1, 1993
Summary
Nitric oxide (NO) can decrease cardiac myocyte contractility. This finding is significant because cardiac cells are very close to blood vessels, suggesting NO
Area of Science:
- Cardiovascular Physiology
- Molecular Cardiology
- Endothelial Function
Background:
- Cardiac muscle fibers are closely associated with microvessels.
- Endothelial-derived factors may influence cardiac myocyte function.
Purpose of the Study:
- To investigate the effects of nitric oxide (NO) and related compounds on cardiac myocyte contractility.
- To determine the mechanism by which NO affects cardiac myocytes.
Main Methods:
- Experiments using isolated, electrically stimulated guinea pig cardiac myocytes.
- Endothelium-myocyte co-culture systems.
- Application of bradykinin, nitrovasodilators, NO solutions, and cyclic GMP analogs.
Main Results:
- Bradykinin reduced myocyte shortening, an effect blocked by NG-nitro-L-arginine methyl ester.
- Sodium nitroprusside and NO solutions attenuated myocyte contraction amplitude.
- The effects of NO were reversed by methylene blue and mimicked by 8-bromoguanosine 3',5'-cyclic monophosphate.
Conclusions:
- Nitric oxide (NO) attenuates cardiac myocyte contractility.
- NO appears to mediate its effects through the production of intracellular guanosine 3',5'-cyclic monophosphate (cGMP).
- Endothelial-derived NO may play a significant role in regulating myocardial function due to the close proximity of myocytes to capillaries.