Effects of sodium gradient manipulation upon cellular calcium ⁴⁵Ca fluxes and cellular sodium in the guinea‐pig taenia coli

Abstract

SUMMARY1. Sucrose and choline were utilized as NaCl substitutes in order to investigate Na-Ca interactions in the smooth muscle of the guinea-pig taenia coli.2. Progressive substitution of NaCl by sucrose caused a progressive increase in cellular exchangeable Ca. This uptake, which amounted to about 300 smole Ca/kg tissue upon total Na replacement, reached a plateau within 20 min. Complete substitution of NaCl by choline chloride caused cellular Ca to increase rapidly to an initial peak, and then decrease to a stable plateau which was also about 300 ,umole/kg above control.3. Replacement of NaCl by either sucrose or choline chloride caused a transient increase in the Ca influx rate, which was measured using a 3 min pulse labelling with 45Ca. This increase was more pronounced in choline chloride.4. NaCl substitution by either sucrose or choline chloride caused a decrease in the 45Ca efflux rate. Two exponential components of transmembrane 45Ca efflux were found in control and Na-free media.5. Treatment of tissues with 3 x 10-5 M-ouabain did not significantly affect the cellular Ca content after 80 min, at which time the Na and K gradients were largely dissipated.6. Removal of medium K caused a slower dissipation of the Na and K gradients. This treatment decreased cellular Ca, did not affect the Ca influx rate, and increased the 45Ca efflux rate.7. Tissues were incubated in depolarizing media containing 10-4 M-ouabain in order to remove the Na gradient. Subsequent measurement of cellular Na indicated the absence of a significant fraction of bound Na.8. The ratio [Na]o/[Na]i had a value of 6-3 in control medium, and decreased as [Na]o was progressively lowered by sucrose substitution, reaching a value of < 1 in a medium containing 5 mm-Na.9. These experiments provide evidence that a Na-Ca exchange carrier does not play an important role in regulation of tension in this muscle, and also indicate that the Ca gradient is not solely dependent on the Na gradient in guinea-pig taenia coli.

Mechanisms involved in contraction of smooth muscles of the rat portal vein as induced by sodium depletion.

“…6A), Na depletion leads to a tonic contraction probably by increasing the influx of Ca. The finding by AARONSON and VAN BREEMEN (1981) that replacement of Na with choline increases cellular Ca, supports this idea. This large tonic contraction may well be a specific response of this vein to Na depletion per se, because re-admission of a small amount of Na relaxed the tissue immediately, and the concentration of choline was kept constant.…”

Effects of calcium and manganese ions on mechanical properties of intact and skinned muscles from the guinea‐pig stomach

“…In the guinea-pig taenia coli, the intracellular Na ion may be diminished after 30 min incubation in the Na-free solution (Brading, 1981;Casteels, 1981). Aaronson & Van Breemen (1981) reported that in 5 mM-Na0, the [Na]0/[Na]i ratio was reduced from 6-3 to > 1, in this same tissue. In different visceral muscles, the [Na]i is estimated the leakage of Ca from the store sites, and effluxes of Ca into the extracellular spaces may also be inhibited.…”

“…The Ca extrusion from smooth muscle cells may require the influx of Na as the Na-Ca exchange process (Reuter, Blaustein & Haeusler, 1973;Blaustein, 1977;Brading, 1978) or the activation of Ca ATPase (Aaronson & Van Breemen, 1981), under physiological conditions. Influxes of Ca in Na-containing solution may also in part be modified by Na ions distributed in the intra-and extra-cellular fluids.…”

Alterations in [Ca2+]i mediated by sodium‐calcium exchange in smooth muscle cells isolated from the guinea‐pig ureter.

“…Although the resulting equilibrium thermodynamic relationship between these gradients has long been appreciated , the physiological significance of the exchange process in many of the various types of cell where it has been observed has remained unclear (van Breemen, Aaronson & Loutzenhiser, 1979;Eisner & Lederer, 1985). It has been suggested, for example, that Na+-Ca2+ exchange is crucial in linking a defect in Na+ metabolism to increased vascular resistance (Blaustein, 1977), but also that the exchange plays little or no part in cellular Ca2+ homeostasis in smooth muscle (Droogmans & Casteels, 1979;Aaronson & van Breemen, 1981; Mulvany, Aalkjaer .…”