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Department of Pharmacology, University of Kentucky College of Medicine, Lexington, Kentucky 40536-0084
The aim of this study was to quantify the contribution of the Na+/H+ exchanger (NHE) and the Na+ channel to the rise in cytosolic Na+ concentration ([Na+]) that is seen in anoxic guinea pig ventricular myocytes. [Na+] was measured with the use of microfluorometry and was found to rise to 44 mM after prolonged anoxia. This rise was partially sensitive to either TTX or HOE-642, selective inhibitors of the Na+ channel and NHE1, respectively. [Na+] did not significantly rise when both drugs were present, suggesting that other routes of Na+ entry were insignificant. However, the relative contributions of the NHE and the Na+ channel were found to be remarkably sensitive to ionic conditions expected to occur during ischemia. The Na+ channel was the dominant Na+ source during acidic anoxia. However, the NHE was the dominant Na+ source during both hyperkalemic anoxia and simulated ischemia (hyperkalemia, low pH, and anoxia). The data suggest that the NHE may prove to be the best pharmacological target to reduce Na+ entry during true ischemia and that inhibition of Na+ influx could contribute strongly to the cardioprotective effects of NHE inhibitors.
heart; sodium; sodium-binding benzofuran isophthalate; ischemia
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