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Published on: February 25, 2016
Induction of persistent sodium current by exogenous and endogenous nitric oxide
G P Ahern1, S F Hsu, V A Klyachko
1Department of Physiology and Biophysics Program, University of Wisconsin, Madison, Wisconsin 53706, USA.
The Journal of Biological Chemistry
|June 2, 2000
Summary
Nitric oxide (NO) directly reduces the inactivation of sodium (Na+) channels, preventing persistent Na+ current in nerve and heart cells. This NO regulation by nitric oxide synthase (NOS) impacts cellular electrical activity.
Area of Science:
- Neuroscience
- Cardiology
- Molecular Biology
Background:
- Voltage-gated Na+ channels typically inactivate, but a persistent Na+ current can remain.
- This persistent current significantly influences excitable cell electrical behavior.
- Mechanisms regulating Na+ channel persistence are poorly understood.
Purpose of the Study:
- To investigate the role of nitric oxide (NO) in regulating persistent Na+ current.
- To elucidate the signaling pathways involved in NO-mediated Na+ channel modulation.
Main Methods:
- Studied Na+ current inactivation in nerve terminals and ventricular myocytes.
- Utilized outside-out patches to examine direct channel effects.
- Measured endogenous NO production using fluorescent dyes.
- Investigated the role of NO synthase (NOS) and its activation by calcium (Ca2+).
Main Results:
- Nitric oxide (NO) was found to reduce Na+ channel inactivation, independent of cGMP.
- The effect of NO was blocked by N-ethylmaleimide, indicating a reactive nitrogen species.
- Endogenous NO, generated by NO synthase (NOS) activated by Ca2+, induced persistent Na+ current.
- NOS inhibitors abolished both NO elevation and persistent Na+ current induction.
Conclusions:
- Nitric oxide (NO) directly regulates Na+ channel inactivation.
- NO acts as a signaling molecule, potentially via reactive nitrogen species.
- NO synthase (NOS) mediates the endogenous production of NO, influencing persistent Na+ current.
- NO is identified as a potential endogenous regulator of persistent Na+ current in physiological and pathophysiological contexts.
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