Cell volume regulation by Amphiuma red blood cells. The role of Ca+2 as a modulator of alkali metal/H+ exchange.

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Abstract
In response to osmotic perturbation, the Amphiuma red blood cell regulates volume back to normal levels. After osmotic swelling, the cells lose K, Cl and osmotically obliged H2O (regulatory volume decrease [RVD]). After osmotic shrinkage, cell volume is regulated as a result of Na, Cl and H2O uptake (regulatory volume increase [RVI]). Ion fluxes responsible for volume regulation are electroneutral, with alkali metal ions obligatorily counter-coupled to H, whereas net Cl flux is in exchange for HCO3. When they were exposed to the Ca ionophore A23187, Amphiuma red blood cells lost K, Cl and H2O with kinetics (time course) similar to those observed during RVD. When cells were osmotically swollen in Ca-free media, net K loss during RVD was inhibited by .apprx. 60%. A role for Ca in the activation of K/H exchange during RVD was suggested from these experiments, but interpretation was complicated by the fact that an increase in cellular Ca resulted in an increase in the membrane conductance to K (GK). To determine the relative contributions of conductive K flux and K/H exchange to total K flux, electrical studies were performed and the correspondence of the net K flux to thermodynamic models for condutive vs. K/H exchange was evaluated. Although Ca activates both condutive and electroneutral K flux pathways, only the latter pathways contribute significantly to net K flux. Since A23187 did not active K loss from cells during RVI (when the Na/H exchange was functioning) and amiloride inhibited K/H exchange by swollen cells only when cells had previously been shrunk in the presence of amiloride, Na/H and K/H exchange are mediated by the same membrane transport moiety.