Abstract
In situ microelectrode examination of rat right atrium showed that in physiologically prestretched tissue, NO donor SNAP modifies the repolarization phase of cardiomyocyte AP in a "hump-like" way provoking the development of arrhythmia. Gadolinium both prevents and eliminates this effect attesting to involvement of stretch-activated channels in the development of NO-induced abnormalities. Elevation of SNAP concentration or further stretch of the tissue (presumably, it increases NO concentration) eliminated the hump depolarization induced by moderate SNAP stimulation. Thus, low NO opens the stretch-activated channels while high NO inactivates them.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
