Key result
In diabetic adult rat ventricular myocytes, the contribution of Na(+)-HCO3- cotransport to total acid-equivalent efflux increased to approximately 58% at pHi 6.75 compared with 33% in normal myocytes.
Absolute Event Rate: 58% vs 33%
Demonstrates that a Cl(-)-independent Na(+)-HCO3- cotransport plays a major role in pH recovery after intracellular acidification in adult rat ventricular myocytes, with an increased relative contribution in diabetic models.
May alter pH recovery in diabetic myocytes; hypothesis-generating for ion transport changes in diabetic cardiomyopathy.
The present work was designed to identify the HCO3(-)-dependent alkalinizing carrier in ventricular myocytes of normal and diabetic adult rats and to determine to what extent this system contributes to acid-equivalent extrusion after an intracellular acidification. We also examined the possible influence of intracellular Ca2+ (Cai2-) and glycolytic inhibition on the carrier activation. Intracellular pH (pHi) was recorded using seminaphthorhodafluor-1. The NH4+ method was used to induce an intracellular acid load. Evidence is provided for the existence of a Cl(-)-independent Na(+)-HCO3- cotransport contributing to pHi recovery from an intracellular acid load in ventricular cells of adult rats. Na(+)-HCO3- cotransport accounts for 33% of the total acid-equivalent efflux (JHe) from normal adult myocytes after intracellular acidification at pHi 6.75 in CO2/HCO3(-)-buffered solution. In addition, the activity of this carrier, which is not affected either by decreasing Cai2+ or by inhibiting Ca2+/calmodulin protein kinase II, is down-regulated by inhibition of glycolysis. Under pathophysiological conditions such as diabetes, although total JHe was significantly decreased compared with normal myocytes, JHe carried by Na(+)-HCO3- cotransport remained unchanged. However, because of a decrease in Na+/H+ exchange, the contribution of this carrier to total JHe increased with decreasing pHi (i.e., under conditions that may be associated with an ischemic episode), reaching approximately 58% of total JHe at pHi 6.75 (vs. approximately 33% in normal myocytes.
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Prigent et al. (1997) studied Normal and diabetic adult rats. Diabetes vs. Normal myocytes was evaluated on Contribution of Na(+)-HCO3- cotransport to total acid-equivalent efflux (JHe) at pHi 6.75. In diabetic adult rat ventricular myocytes, the contribution of Na(+)-HCO3- cotransport to total acid-equivalent efflux increased to approximately 58% at pHi 6.75 compared with 33% in normal myocytes.
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