Ouabain inhibits intracellular pH recovery from acidosis in cultured mouse heart cells.
Myocardial ischaemia induces cytosolic acidification, which promotes cardiac damage, dysfunction or arrhythmia. In this study, we investigated the effect of ouabain on the intracellular pH (pHi) in cultured mouse ventricular cells, using 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein (BCECF). The average resting pHi in myocytes was 7.19. After myocytes were acid-loaded with NH4Cl, the pHi recovered from acidosis to the resting level within a few minutes via amiloride-sensitive Na+/H+ exchange. Ouabain inhibited this pHi recovery dose-dependently with half-maximal inhibition at 3 X 10(-5) M, but did not suppress the ionophore monensin-induced pHi elevation. The inhibition of the pHi recovery from acidosis by ouabain is possibly caused by an inhibition of amiloride-sensitive Na+/H+ exchange, which is secondary to a suppression of Na+ efflux through (Na+, K+) pump. Above results demonstrate the possibility that digitalis promotes intracellular acidosis or inhibits the pHi recovery from acidosis in ischaemic myocardium.
Arisaka
H
H
Department of Cardiology, Jichi Medical School, Tochigi, Japan.
Ikeda
U
U
Takayasu
T
T
Takeda
K
K
Natsume
T
T
Hosoda
S
S
D000138:Acidosis / Q000503:physiopathology*; D000818:Animals; D002478:Cells, Cultured; D006863:Hydrogen-Ion Concentration; D007474:Ion Exchange; D051379:Mice; D009206:Myocardium / Q000166:cytology / Q000378:metabolism* / Q000473:pathology; D010042:Ouabain / Q000494:pharmacology*; D012964:Sodium / Q000502:physiology
D010042:Ouabain; D012964:Sodium