Calcium current in isolated neonatal rat ventricular myocytes.

Abstract

1. Calcium currents (ICa) from neonatal rat ventricular heart muscle cells grown in primary culture were examined using the 'whole‐cell' voltage‐clamp technique (Hamill, Marty, Neher, Sakmann & Sigworth, 1981). Examination of ICa was limited to one calcium channel type, 'L' type (Nilius, Hess, Lansman & Tsien, 1985), by appropriate voltage protocols. 2. We measured transient and steady‐state components of ICa, and could generally describe ICa in terms of the steady‐state activation (d infinity) and inactivation (f infinity) parameters. 3. We observed that the reduction of ICa by the calcium channel antagonist D600 can be explained by both a shift of d infinity to more positive potentials as well as a slight reduction of ICa conductance. D600 did not significantly alter either the rate of inactivation of ICa or the voltage dependence of f infinity. 4. The calcium channel modulator BAY K8644 shifted both d infinity and f infinity to more negative potentials. Additionally, BAY K8644 increased the rate of inactivation at potentials between +5 and +55 mV. Furthermore, BAY K8644 also increased ICa conductance, a change consistent with a promotion of 'mode 2' calcium channel activity (Hess, Lansman & Tsien, 1984). 5. We conclude that, as predicted by d infinity and f infinity, there is a significant steady‐state component of ICa ('window current') at plateau potentials in neonatal rat heart cells. Modulation of the steady‐state and transient components of ICa by various agents can be attributed both to specific alterations in d infinity and f infinity and to more complicated alterations in the mode of calcium channel activity.

On the Role of Ca 2+ - and Voltage-Dependent Inactivation in Ca v 1.2 Sensitivity for the Phenylalkylamine (-)Gallopamil

“…(1) In line with earlier studies, 26,27 we found no drug-induced acceleration of the Ca 2ϩ -dependent component of I Ca decay ( Figures 4A and 4C). (2) The kinetics of recovery from Ca 2ϩ -dependent inactivation were unaffected even by high drug concentrations (50 to 100 mol/L, Figure 6).…”

“…[2][3][4]7,8,26,27,34 A high-affinity drug binding to the inactivated channel state would result in a substantial shift of the inactivation curve to more negative potentials. However, if the inactivation curve is measured under conditions close to steady-state the observed shift is hardly significant 35 (see also Aczel et al 10 and Degtiar et al 36 for an overview of the steady-state problem).…”

Effects of captopril on membrane current and contraction in single ventricular myocytes from guinea‐pig

“…The shift of the d. variable is small and is in the opposite direction to that reported to occur on exposure to the phenylalkylamine calcium antagonists. For example Cohen & Lederer (1987) found that D600 produced a positive shift of this variable in neonatal rat ventricular myocytes. On the other hand these workers and Fox et al (1987) found that the dihydropyridine agonist Bay K 8644 gives rise to a negative shift of the activation curve.…”

“…On the other hand these workers and Fox et al (1987) found that the dihydropyridine agonist Bay K 8644 gives rise to a negative shift of the activation curve. We may rule out the possibility that inhibition of nearonal catecholamine release is involved since isolated myocytes are effectively denervated (Dow et al, 1981) and the effects of the drug on the activation variable are not those which would be expected from reversal of /-adrenoceptor stimulation (Cohen & Lederer, 1987). Angiotensin II increases the calcium current in neonatal rat ventricular myocytes (Allen et al, 1987).…”

Contribution of Sarcoplasmic Reticulum Ca2+ Release and Ca2+ Transporters on Sarcolemmal Channels to Ca2+ Transient in Fetal Mouse Heart

“…Ventricular myocytes were enzymatically isolated from fetal mouse hearts (24,25). Fetal mice at ED 14.5 were taken out, and the hearts were quickly removed.…”