Résumé
The effects of short (1 min) and long (7–10 min) exposure to hyposmotic solution on excitation-contraction coupling in rat ventricular myocytes were studied. After short exposure, the action potential duration at 90% repolarization (APD 90 ), the intracellular Ca 2+ concentration ([Ca 2+ ] i ) transient amplitude, and contraction increased, whereas the L-type Ca 2+ current ( I Ca,L ) amplitude decreased. Fractional sarcoplasmic reticulum (SR) Ca 2+ release increased but SR Ca 2+ load did not. After a long exposure, I Ca,L , APD 90 , [Ca 2+ ] i transient amplitude, and contraction decreased. The abbreviation of APD 90 was partially reversed by 50 μM DIDS, which is consistent with the participation of Cl − current activated by swelling. After 10-min exposure to hyposmotic solution in cells labeled with di-8-aminonaphthylethenylpyridinium, t-tubule patterning remained intact, suggesting the loss of de-t-tubulation was not responsible for the fall in I Ca,L . After long exposure, Ca 2+ load of the SR was not increased, and swelling had no effect on the site-specific phosphorylation of phospholamban, but fractional SR Ca 2+ release was depressed. The initial positive inotropic response to hyposmotic challenge may be accounted for by enhanced coupling between Ca 2+ entry and release. The negative inotropic effect of prolonged exposure can be accounted for by shortening of the action potential duration and a fall in the I Ca,L amplitude.