Normal contractions triggered by I(Ca,L) in ventricular myocytes from rats with postinfarction CHF.
I. Sjaastad, J. B�kenes, F. Swift, J. Wasserstrom, and O. Sejersted.
Am. J. Physiol. Heart Circ. Physiol. 283 (3): H1225-36 (September 2002)

Attenuated L-type Ca$^2+$ current (I(Ca,L)), or current-contraction gain have been proposed to explain impaired cardiac contractility in congestive heart failure (CHF). Six weeks after coronary artery ligation, which induced CHF, left ventricular myocytes from isoflurane-anesthetized rats were current or voltage clamped from -70 mV. In both cases, contraction and contractility were attenuated in CHF cells compared with cells from sham-operated rats when cells were only minimally dialyzed using high-resistance microelectrodes. With patch pipettes, cell dialysis caused attenuation of contractions in sham cells, but not CHF cells. Stepping from -50 mV, the following variables were not different between sham and CHF, respectively: peak I(Ca,L) (4.5 +/- 0.3 vs. 3.8 +/- 0.3 pApF(-1) at 23 degrees C and 9.4 +/- 0.5 vs. 8.4 +/- 0.5 pApF(-1) at 37 degrees C), the bell-shaped voltage-contraction relationship in Cs$^+$ solutions (fractional shortening, 15.2 +/- 1.0\% vs. 14.3 +/- 0.7\%, respectively, at 23 degrees C and 7.5 +/- 0.4\% vs. 6.7 +/- 0.5\% at 37 degrees C) and the sigmoidal voltage-contraction relationship in K$^+$ solutions. Caffeine-induced Ca$^2+$ release and sarcoplasmic reticulum Ca$^2+$-ATPase-to-phospholamban ratio were not different. Thus CHF contractions triggered by I(Ca,L) were normal, and the contractile deficit was only seen in undialyzed cardiomyocytes stimulated from -70 mV.
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