Normal contractions triggered by I_Ca,L in ventricular myocytes from rats with postinfarction CHF

Attenuated L-type Ca²⁺ 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 shamoperated 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°C and 9.4 ± 0.5 vs. 8.4 ± 0.5 pApF^-1 at 37°C), the bell-shaped voltage-contraction relationship in Cs⁺ solutions (fractional shortening, 15.2 ± 1.0% vs. 14.3 ± 0.7%, respectively, at 23°C and 7.5 ± 0.4% vs. 6.7 ± 0.5% at 37°C) and the sigmoidal voltage-contraction relationship in K⁺ solutions. Caffeine-induced Ca²⁺ release and sarcoplasmic reticulum Ca²⁺-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.