LACTIC-ACIDOSIS TRANSIENTLY INCREASES METABOLIC-RATE OF TURTLE MYOCYTES

We measured O-2 consumption as an estimate of metabolic rate in isolat ed calcium-tolerant ventricular myocytes of turtles (Chrysemys picta b elli) at control pH 7.8 and in the same solution brought to pH 7.4 and 7.0 with additions of lactic acid. Our aim was to test the hypothesis that lactic acidosis caused metabolic depression by initiating downre gulation of Na+ channels, and thus Na+-K+-ATPase (Na+ pump) activity, which we would measure as a decrease in O-2 consumption. Myocyte O-2 c onsumption was measured in reptilian N-tris(hydroxymethyl)methyl-2-ami noethanesulfonic acid-buffered Ringer solution and in nominally Na+- a nd Ca2+-free solution, thus estimating the Na+ pump component of metab olic rate. Lowering extracellular pH from 7.8 to 7.0 resulted in a sig nificant increase in metabolic rate of cells in Ringer solution but no t those in Na+- and Ca2+-free solution. This result was unchanged by t he addition of 2 mM Ca2+ to Na+-free cell suspensions, indicating that the difference was due to the presence of Na+. Addition of 100 mu M a miloride to cells in Ringer solution at pH 7.0 abolished the increase in O-2 consumption, suggesting that the apparent increase in Na+-K+-AT Pase activity was secondary to Na+-H+ exchange. Intracellular pH was m easured using 5,5-dimethyl[C-14]oxazolidine-2,4-dione. Cells treated w ith amiloride and those in Na+- and Ca2+-free solution did not regulat e intracellular pH following acidosis and maintained basal metabolic r ate. These data suggest that the Na+-H+ exchanger is an important cont ributor to intracellular pH regulation in the myocyte but increases Na + pump activity and metabolic rate immediately following acidosis.