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Am J Physiol Heart Circ Physiol (April 11, 2002). doi:10.1152/ajpheart.00198.2002
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Articles in PresS, published online ahead of print April 11, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00198.2002
Submitted on March 6, 2002
Accepted on April 5, 2002

H2O2-Induced Ca2+ Overload in Ventricular Myocytes Involves ERK1/2 MAP Kinases: Role for NHE-1 Dependent and Independent Pathways

Emily C. Rothstein1, Kenneth L. Byron2, Ryan E. Reed1, Larry Fliegel3, and Pamela A. Lucchesi1*

1 Physiology and Biophysics, University Alabama Birmingham, Birmingham, AL, USA
2 Medicine and Cardiovascular Institute, Loyola University Chicago, Maywood, IL, USA
3 Biochemistry, University Alberta Edmonton, Edmonton, Alberta, Canada

* To whom correspondence should be addressed. E-mail: lucchesi{at}physiology.uab.edu.

Generation of reactive oxygen species (ROS) and intracellular Ca2+ overload are key mechanisms involved in ischemia/reperfusion (I/R)-induced myocardial injury. The relationship between I/R injury and Ca2+ overload has not been fully characterized. The increase in Na+/H+ exchanger (NHE-1) activity observed during I/R injury is an attractive candidate to link increased ROS production with Ca2+ overload. We have previously shown that low doses of H2O2 increase NHE-1 activity in an extracellular signal-regulated kinase (ERK)-dependent manner. In this paper, we examined the effect of low doses of H2O2 on intracellular Ca2+ in Fura-2 loaded, spontaneously contracting neonatal rat ventricular myocytes. H2O2 induced a time- and concentration-dependent increase in diastolic [Ca2+]i that was blocked by inhibition of ERK1/2 activation with 5µM U0126 (88%) or inhibition of NHE-1 with 5µM HOE642 (50%). Increased NHE activity was associated with phosphorylation of the NHE-1 carboxy tail that was blocked by U0126. These results suggest that H2O2-induced Ca2+ overload is partially mediated by NHE-1 activation secondary to phosphorylation of NHE-1 by the ERK1/2 MAP kinase pathway.




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