Na/H exchange in cultured chick heart cells: secondary stimulation of electrogenic transport during recovery from intracellular acidosis.
Intracellular acidosis is capable of stimulating a rapid amiloride-sensitive Na/H exchange mechanism in the cell membrane of cultured chick heart cells. The sequence of changes of intracellular sodium and potassium contents during recovery from an acid load in heart cells was determined by atomic absorption spectrophotometry and correlated with electrophysiological measurements. Induction of an intracellular acid load by removal of NH4Cl from the bathing solution caused a rapid rise in sodium content that was amiloride-sensitive. Following a peak, sodium content declined concomitant with a rise in potassium content; these changes were ouabain-sensitive and corresponded with a ouabain-sensitive membrane hyperpolarization beyond the calculated potassium equilibrium potential. These observations indicate that pHi regulation in cardiac muscle, following an intracellular acid load involves extrusion of H+ by electroneutral Na/H exchange with the consequent rise in Nai stimulating the electrogenic Na/K pump to return Nai to control level. In the presence of amiloride (10(-4) M), the hyperpolarization was slower although still present: this suggests the existence of another sodium uptake mechanism which contributes to stimulation of electrogenic transport.
D000200:Action Potentials; D000584:Amiloride / Q000494:pharmacology; D000818:Animals; D001692:Biological Transport; D002478:Cells, Cultured; D002642:Chick Embryo; D006863:Hydrogen-Ion Concentration; D009206:Myocardium / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism; D011522:Protons; D000644:Quaternary Ammonium Compounds / Q000378:metabolism; D012964:Sodium / Q000378:metabolism*
D011522:Protons; D000644:Quaternary Ammonium Compounds; D000584:Amiloride; D012964:Sodium; D011188:Potassium