title: The control of the contraction of myocytes from guinea-pig heart by the resting membrane potential.
abstract: 1. 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.
authors.affiliation: Institut für Pharmakologie und Toxikologie, Technischen Universität München, Germany.
authors.forename: J
authors.initials: J
authors.lastname: Mermi
authors.forename: M
authors.initials: M
authors.lastname: Yajima
authors.forename: F
authors.initials: F
authors.lastname: Ebner
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism; D002462:Cell Membrane / Q000187:drug effects / Q000502:physiology; D006168:Guinea Pigs; D006321:Heart / Q000502:physiology*; D066298:In Vitro Techniques; D007474:Ion Exchange; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009200:Myocardial Contraction / Q000502:physiology*; D009206:Myocardium / Q000166:cytology*; D012039:Regional Blood Flow / Q000502:physiology; D012964:Sodium / Q000378:metabolism / Q000494:pharmacology; D013623:Tail / Q000098:blood supply
chemical_list: D012964:Sodium; D002118:Calcium