Altered jejunal potassium (Rb+) transport in piglet rotavirus enteritis.

To determine the mechanisms of K+ loss in viral diarrhea, K+ fluxes (estimated by tracer Rb+ flows) across piglet jejunum in Ussing chambers were determined. Normal jejunum was characterized by an indomethacin-sensitive short-circuit current and a small K+ secretory flow. Rotavirus-infected gut secreted K+ at high rates, probably resulting from increased prostaglandin generation because secretion was abolished by indomethacin. Tissues pretreated with indomethacin responded to 8-bromoadenosine 3',5'-cyclic monophosphate acid and 16,16-dimethyl-prostaglandin E2 with K+ secretion. The secretory response in rotavirus-infected jejunum was no greater than that in normal tissue. Serosal addition of Ca2+ ionophore A23187 caused K+ secretion in normal but not rotavirus-infected jejunum. To inhibit the basolateral uptake of K+ and reduce the driving force for secretion, ouabain was added to the bath. Ouabain unmasked a K+ absorptive process in normal intestine, which was not seen in rotavirus-infected tissue. K+ absorption was inhibited by 3-(cyanomethyl)-2-methyl-8-(phenyl-methoxy)imidazo (1,2 alpha)pyridine (Sch-28080) and omeprazole. We speculate that the high fecal K+ losses observed in human rotavirus enteritis might be caused by an imbalance between K+ secretion and an impaired apical K+ absorptive mechanism in the crypt-type epithelium.