Calcium‐sodium antagonism on the frog's heart: a voltage‐clamp study.

Abstract

6. In Na-free choline-Ringer, a strong contracture developed followed by a spontaneous relaxation. Starting from the relaxed state, application of depolarizing clamps gave rise to phasic contractions with a very slow relaxation while tonic contractions were apparently lacking.7. The results are interpreted in terms of an energy-dependent carrier mechanism exchanging one Ca for two Na ions across the cell membrane. The model implies a strong asymmetry in the rate constants governing the chemical reactions on both sides of the membrane. The system is thought to operate close to equilibrium at any potential, thereby determining the * Send reprint requests to Professor H. G. Haas.6. BENNINGER AND OTHERS steady level of myoplasmic Ca. The equilibrium itself is considered to shift upon depolarization. Assuming that [Na]i is constant, the steady level of [Ca], is expected to be proportional to the [Ca]o/[Na]2 ratio, the scale factor being a function of membrane potential.8. The carrier model suggests the occurrence of a depolarization-induced inward transfer of Ca which might be involved in the generation of tonic contractions.9. The apparent lack of tonic contractions in the absence of external Na ions may be explained by a suppression of carrier-mediated Ca influx normally occurring upon depolarization.10. The antagonistic effects of [Ca]o and [Na]o on phasic contraction are understood as being due to alterations of the Ca pumping system rather than changes in slow inward current.

"Creep currents" in single frog atrial cells may be generated by electrogenic Na/Ca exchange.

“…Attempts in frog atrium have relied upon examination of ionic currents before and after changes in [Na],, or [Ca]o. Benninger et al (1976) failed to detect any measurable change in current in response to a reduction in [Na]o, but the recent data of Mentrard et al (1984), using a similar experimental procedure, revealed small changes in membrane current that were considered to be consistent with the thermodynamic model of electrogenic Na/Ca exchange proposed by Mullins (1979) . However, any change in the Na/Ca exchange current under these conditions must be quite transient in nature, and would have to be measured quickly, before subsequent changes in [Na] ; could occur (Ellis and Deitmer, 1978).…”

Sodium and calcium fluxes in a clonal nerve cell line.

“…Rink (1977) found no evidence that the Na+-Ca2+ exchange in adrenal medulla could be reversed to give Ca2+ influx. Furthermore, the available evidence shows that Na+-Ca2+ exchange is insensitive to inhibition by C02+ and Mn24 (Rink, 1977; Benninger, Einwlichter, Haas & Kern, 1976). Therefore, even if Ca2+ uptake does occur via a reversal of Na+-Ca+2 exchange we should be able to distinguish it from voltage-dependent Ca2+fluxwhichisinhibitedbylow concentrations of C02+ and Mn2+.…”

Influence of potassium, sodium, perfusion pressure, and isoprenaline on renin release induced by acute calcium deprivation

“…An exchange mechanism between Na and Ca has been observed in other cells, most notably, muscle, nerve, and endocrine. For example, in those cells lowering extracellular Na concentration raises cytoplasmic Ca which then triggers contraction, excitation, and secretion (Brading, 1978;Aguirre, Pinto & Trifaro, 1977;Blaustein, 1974Blaustein, , 1977Ma & Bose, 1977;Baker, 1972Baker, , 1976Baker & McNaughton, 1976;Benninger, Einwachter, Hass & Kern, 1976;Cochrane & Douglas, 1976;Lestowecka & Trifaro, 1974;Reuter, Blaustein & Haeusler, 1973;Reuter & Seitz, 1968). Conversely, in the juxtaglomerular cells lowering extracellular Na raises cytoplasmic concentration of Ca which then inhibits release of renin.…”