Long-term acclimation of Mytilus californianus to 60% artificial sea water (585 mosmol l-1; ASW) led to a 30-40% decrease in the taurine (53.5-36.9 mumol g-1 wet mass) and betaine (44.8-26.2 mumol g-1 wet mass) content of gill tissue, compared with that of control animals held in 100% ASW (980 mosmol l-1). The K+ content of gills did not change following long-term acclimation to reduced salinity. In contrast, losses of all three solutes during a brief (60 min) exposure to 60% ASW were less than or equal to 15%. Nevertheless, the swelling of gill cells that occurred after acute exposure to 60% ASW was followed by a return towards the control volume. Direct optical measurement of single gill filaments confirmed that, during an acute exposure to reduced salinity, ciliated lateral cells increased in cell height (volume) and then underwent a regulatory volume decrease (RVD) with a half-time of approximately 10 min. This short-term RVD was completely inhibited by exposure to 1 mmol l-1 quinidine, a K+ channel blocker, but only when the drug was applied to the basolateral aspect of the gill epithelium. Application of 1 mumol l-1 valinomycin relieved the inhibition by quinidine of the gill RVD. However, addition of valinomycin did not accelerate the rate of RVD observed in the absence of quinidine. These results indicate that long-term acclimation of Mytilus californianus gill in dilute sea water involves primarily losses of taurine and betaine, whereas short-term regulation of cell volume may involve an electrically conductive loss of intracellular K+ and a counter ion.

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