The sodium-calcium relationship in mammalian myocardium: Effect of sodium deficient perfusion on calcium fluxes

Calcium exchange in the isolated, arterially-perfused interventricular septum of the rabbit was studied under conditions of varying levels of sodium deficient perfusion and supports the concept that, in cardiac muscle, alterations in the [Na] 1 /[Na] o ratio modify contractile force through a primary effect on Ca influx.

Abstract

Calcium exchange in the isolated, arterially-perfused interventricular septum of the rabbit was studied under conditions of varying levels of sodium deficient perfusion. Reduction of [Na]o was associated with a net gain in tissue Ca. With reduction of [Na]o to 36, 12 and 0 mm the net gain in Ca was respectively, 0.896±0.116 (s.e.m.), 1.240±0.057 and 1.546±0.036 mmol kg−1 dry tissue wt. 45Ca washout experiments revealed that Ca efflux was unaltered during perfusion with 36 mm [Na]o. When [Na]o was reduced to 12 mm a slight depression of Ca efflux was observed and at 0 mm [Na]o there was clear evidence of substantial inhibition of Ca efflux. Studies in heart cell culture confirmed the inhibition of Ca efflux during zero [Na]o perfusion. In these experiments the rate of Ca efflux was depressed by an average 27.8% when [Na]o was reduced to zero. Although the results support the existence, in cardiac muscle, of a component of Ca efflux which is dependent on external Na they also indicate that this mechanism is essentially fully saturated at relatively low [Na]o (<36 mm). Ca influx, however, appears to be considerably more sensitive to reduction of [Na]o This supports the concept that, in cardiac muscle, alterations in the [Na]1/[Na]o ratio modify contractile force through a primary effect on Ca influx. Calcium exchange in the isolated, arterially-perfused interventricular septum of the rabbit was studied under conditions of varying levels of sodium deficient perfusion. Reduction of [Na]o was associated with a net gain in tissue Ca. With reduction of [Na]o to 36, 12 and 0 mm the net gain in Ca was respectively, 0.896±0.116 (s.e.m.), 1.240±0.057 and 1.546±0.036 mmol kg−1 dry tissue wt. 45Ca washout experiments revealed that Ca efflux was unaltered during perfusion with 36 mm [Na]o. When [Na]o was reduced to 12 mm a slight depression of Ca efflux was observed and at 0 mm [Na]o there was clear evidence of substantial inhibition of Ca efflux. Studies in heart cell culture confirmed the inhibition of Ca efflux during zero [Na]o perfusion. In these experiments the rate of Ca efflux was depressed by an average 27.8% when [Na]o was reduced to zero. Although the results support the existence, in cardiac muscle, of a component of Ca efflux which is dependent on external Na they also indicate that this mechanism is essentially fully saturated at relatively low [Na]o (<36 mm). Ca influx, however, appears to be considerably more sensitive to reduction of [Na]o This supports the concept that, in cardiac muscle, alterations in the [Na]1/[Na]o ratio modify contractile force through a primary effect on Ca influx.