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Am J Physiol Heart Circ Physiol 273: H2596-H2603, 1997;
0363-6135/97 $5.00
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Vol. 273, Issue 6, H2596-H2603, December 1997

HCO<SUP>−</SUP><SUB>3</SUB>-dependent alkalinizing transporter in adult rat ventricular myocytes: characterization and modulation

Karine Le Prigent1, Dominique Lagadic-Gossmann2, Emmanuel Mongodin1, and Danielle Feuvray1

1 Laboratoire de Physiologie Cellulaire, Université Paris XI, 91405 Orsay cedex; and 2 Institut National de la Santé et de la Recherche Médicale U456, Faculté de Pharmacie, 35043 Rennes cedex, France

The present work was designed to identify the HCO<SUP>−</SUP><SUB>3</SUB>-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+ (Ca2+i) and glycolytic inhibition on the carrier activation. Intracellular pH (pHi) was recorded using seminaphthorhodafluor-1. The NH+4 method was used to induce an intracellular acid load. Evidence is provided for the existence of a Cl--independent Na+-HCO<SUP>−</SUP><SUB>3</SUB> cotransport contributing to pHi recovery from an intracellular acid load in ventricular cells of adult rats. Na+-HCO<SUP>−</SUP><SUB>3</SUB> cotransport accounts for 33% of the total acid-equivalent efflux (JeH) from normal adult myocytes after intracellular acidification at pHi 6.75 in CO2/HCO<SUP>−</SUP><SUB>3</SUB>-buffered solution. In addition, the activity of this carrier, which is not affected either by decreasing Ca2+i or by inhibiting Ca2+/calmodulin protein kinase II, is downregulated by inhibition of glycolysis. Under pathophysiological conditions such as diabetes, although total JeH was significantly decreased compared with normal myocytes, JeH carried by Na+-HCO<SUP>−</SUP><SUB>3</SUB> cotransport remained unchanged. However, because of a decrease in Na+/H+ exchange, the contribution of this carrier to total JeH increased with decreasing pHi (i.e., under conditions that may be associated with an ischemic episode), reaching ~58% of total JeH at pHi 6.75 (vs. ~33% in normal myocytes).

sodium-bicarbonate cotransport; cardiac ventricular myocytes; streptozotocin-induced diabetes; intracellular calcium; glycolysis inhibition


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