Abstract
We used genetically modified mice to test the hypothesis that pH regulation of the cardiac sodium calcium-exchanger (NCX1) contributes to ischemia/reperfusion (I/R) injury. NCX1 is the dominant calcium (Ca) efflux mechanism of cardiomyocytes and is strongly regulated by pH. During ischemia, when pH is lowered by anaerobic glycolysis, inhibition of NCX1 by acidosis may potentiate the Na overload imposed by Na/K pump failure and Na-H exchange. Upon reperfusion and restoration of normal pH, this high intracellular Na concentration drives the now functional NCX1 into reverse mode resulting in Ca overload.
Sign-in/Register to access full text options 
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.
