Peripheral blood T lymphocytes swollen in hypotonic media regain normal size by releasing internal KCl through activation of conductive K+ and Cl- pathways. In contrast, no regulatory volume decrease (RVD) is observed in tonsillar B lymphocytes. The volume-induced K+ permeability is minimal in these cells, but little was known about the effect of swelling on anion transport and its coupling to cation translocation. The induction of an anion-conductive pathway on swelling of B cells was demonstrated in the following way: 1) when an exogenous cation ionophore was added, hypotonic swelling was followed by secondary volume changes, the direction of which was dictated by the electrochemical gradients of the diffusible ions; 2) the rate of 36Cl efflux was markedly increased by swelling; and 3) upon swelling, the membrane potential approached the Cl- equilibrium potential. Quinine, which blocks K+ transport and RVD in swollen T cells, has no effect on volume-induced anion fluxes. Consequently, secondary volume changes could be elicited by gramicidin in cells pretreated with quinine. It can be concluded that in B cells, swelling leads to activation of a conductive Cl- permeability but not of K+ permeability. These and other findings support the view that the Cl- pathway functions independently of the K+ pathway.
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