Chloride self-exchange in toad skeletal muscle in vivo and in vitro.

The exchange of cellular Cl with 36Cl has been measured in saline-perfused hindlimb muscles of the pithed toad and compared with cellular Cl exchange in isolated muscles incubated in the vitro either in toad Ringer solution or in toad plasma. In the perfused hindlimb, the rate of 36Cl efflux from muscle cells [17.0 +/- 0.9 pmol Cl.(cm2 plasma membrane.s)-1] was only 40% as fast as that of the 36Cl influx. The discrepancy between Cl influx and efflux was accompanied by a cellular accumulation of Cl against the electrochemical gradient for this anion. Concurrently, the cells took up Na in amounts at least equal to the accumulated Cl. During this accumulation of Na and Cl, the mean resting potential remained constant at a value of -89.2 +/- 1.9 (SE) mV. Na and Cl were taken up by the muscle cells of the perfused hindlimb without a concomitant decrease in cellular K content; i.e., without evidence of inhibition of the Na-K pump. The rate constant for cellular 36Cl efflux from isolated toad muscles preincubated for 3 h in vitro in toad Ringer solution was about five times faster than that of muscles in the perfused hindlimb and similar in magnitude to published values for Cl fluxes in frog muscle. Cellular Cl efflux from muscles briefly preincubated in vitro for 15 min instead of 3 h was significantly slower than after prolonged preincubation. In vitro incubation of isolated toad muscles in toad plasma slowed the cellular 36Cl efflux to values approaching those measured in the perfused hindlimb, without comparably depressing the 36Cl influx. It is suggested that the uptake of NaCl by the cells of perfused hindlimb muscle may proceed by an electroneutral inward cotransport of Na and Cl on the same carrier.