F. Brette et al., Biphasic effects of hyposmotic challenge on excitation-contraction coupling in rat ventricular myocytes, AM J P-HEAR, 279(4), 2000, pp. H1963-H1971
Citations number
40
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
The effects of short (1 min) and long (7-10 min) exposure to hyposmotic sol
ution on excitation-contraction coupling in rat ventricular myocytes were s
tudied. After short exposure, the action potential duration at 90% repolari
zation (APD(90)), the intracellular Ca2+ concentration ([Ca2+](i)) transien
t amplitude, and contraction increased, whereas the L-type Ca2+ current (I-
Ca,I- L) amplitude decreased. Fractional sarcoplasmic reticulum (SR) Ca2+ r
elease increased but SR Ca2+ load did not. After a long exposure, I-Ca,I- L
, APD(90), [Ca2+](i) transient amplitude, and contraction decreased. The ab
breviation of APD(90) was partially reversed by 50 mu M DIDS, which is cons
istent with the participation of Cl- current activated by swelling. After 1
0-min exposure to hyposmotic solution in cells labeled with di-8-aminonapht
hylethenylpyridinium, t-tubule patterning remained intact, suggesting the l
oss of de-t-tubulation was not responsible for the fall in I-Ca,I- L. After
long exposure, Ca2+ load of the SR was not increased, and swelling had no
effect on the site-specific phosphorylation of phospholamban, but fractiona
l SR Ca2+ release was depressed. The initial positive inotropic response to
hyposmotic challenge may be accounted for by enhanced coupling between Ca2
+ entry and release. The negative inotropic effect of prolonged exposure ca
n be accounted for by shortening of the action potential duration and a fal
l in the I-Ca,I- L amplitude.