Article date: November 1991
By: J. Mermi, M. Yajima, F. Ebner, in Volume 104, Issue 3, pages 705-713
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.
While ineffective at 140 and 5 mmol 1−1 [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 1−1). Elevated intracellular Na+ after Na+‐pump inhibition with ouabain 1–10 μmol 1−1 was similarly effective with regard to the inotropic response to different holding potentials.
At − 70 mV holding potential, reduction of [Na+]o from 140 to 70 mmol 1−1 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 Ni2+‐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.
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.
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.
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.
While ineffective at 140 and 5 mmol 1−1 [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 1−1). Elevated intracellular Na+ after Na+‐pump inhibition with ouabain 1–10 μmol 1−1 was similarly effective with regard to the inotropic response to different holding potentials.
At − 70 mV holding potential, reduction of [Na+]o from 140 to 70 mmol 1−1 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 Ni2+‐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.
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.
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.
DOI: 10.1111/j.1476-5381.1991.tb12492.x
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