The effect of cell swelling and cell shrinkage on K+ transport across the r
at colonic epithelium was studied by measuring unidirectional fluxes, uptak
e and efflux of Rb-86(+), a marker for K+. Exposure to a hypotonic medium s
timulated the secretory, serosa-to-mucosa flux of K+, whereas exposure to a
hypertonic medium inhibited the absorptive, mucosa-to-serosa flux of K+ in
the distal, but not in the proximal colon. Neither manoeuvre had any effec
t on the uptake of K+ across the apical or the basolateral membrane. Cell s
welling induced a sustained increase in the apical and basolateral K+ efflu
x from both colonic segments, whereas cell shrinkage reduced the efflux. Ba
2+ (10(-2) mol l(-1)) inhibited the swelling-induced stimulation of the api
cal, quinine (10(-3) mol l(-1)) that of the basolateral K+ efflux in the di
stal colon. Incubation of the tissue in Ca2+-free buffer or La3+, which blo
cks Ca2+-influx into the epithelium, strongly reduced the basal K+ efflux a
cross the basolateral membrane. The same was observed with brefeldin A, a b
locker of the transport of newly synthesized proteins out of the endoplasma
tic reticulum. Swelling-induced K+ efflux, however, was not reduced. In the
presence of colchicine, an inhibitor of the polymerization of microtubules
, swelling evoked only a transient increase in mucosal efflux, which, espec
ially in the proximal colon, fell after 6 min to the level of the isotonic
control period. These results demonstrate that the cell volume is involved
in the regulation of transepithelial K+ transport across the rat colonic ep
ithelium and suggest a role of the cytoskeleton in the control of a part of
the volume-sensitive K+ channels.