Key points are not available for this paper at this time.
The influence of different holding potentials (-120 to -70 mV) on the contraction of enzymatically dispersed myocytes from guinea-pig hearts was evaluated. Contractions were elicited by repetitive depolarizations to 0 mV at 0.5 Hz. 2. While ineffective at 140 and 5 mmol l-1 Na+o and pipette Na+, respectively, depolarization of the resting membrane with the holding potential increased myocyte shortening at reduced Na+ gradients (Na+o 70 or Na+i 10-15 mmol l-1). Elevated intracellular Na+ after Na(+)-pump inhibition with ouabain 1-10 mumol l-1 was similarly effective with regard to the inotropic response to different holding potentials. 3. At -70 mV holding potential, reduction of Na+o from 140 to 70 mmol l-1 increased myocyte shortening and induced an inwardly directed component of the holding current which peaked at -44 +/- 10 pA and declined thereafter in parallel with the inotropic effect. The relation of this inward current to Ca2+i was confirmed by experiments at high Ca2+ buffer capacity where Na+o reduction induced a Ni(2+)-insensitive, outwardly directed component (36 +/- 15 pA) of the holding current. The observed inward current is suggested to reflect the extrusion of Ca2+i in exchange for Na+o as a counter-regulatory mechanism which limits the increase of Ca2+i. 4. The interventions which increased the strength of the contraction also enhanced the transient tail current after repolarization, suggesting its close relation to Ca2+i. This finding confirmed the pattern found with cell shortening. 5. It is concluded that under certain conditions, voltage-dependent and Na(+)-dependent Na(+)-Ca2+ exchange during the interval between the contractions is relevant to the diastolic concentration of Ca2+i which in turn determines the accumulation of Ca2+ in the sarcoplasmic reticulum and the magnitude of the subsequent contraction.
Mermi et al. (Fri,) studied this question.