Studies on kallikreins. VII. Effects of kallikrein and some autacoids on in vitro transport of valine and sodium ion.

Abstract

The effect of kallikrein and some autacoids on the transport and uptake of valine in the rat small intestine was examined, in vitro, by the method of sac of everted in testine and by measurement of uptake of valine in the tissue. Kallidin and rat intestinal kallikrein (RIK) stimulated the intestinal transport of valine, like bradykinin and pancreatic kallikrein. Kallidin was more effective than bradykinin or Met-Lys-bradykinin. RIK stimulated the transport significantly when it was added to either the mucosal or serosal side. Moreover, the accumulation of valine into the small intestine was enhanced by bradykinin, and a similar result was obtained by the combined addition of rat pancreatic kallikrein and rat kininogen to the medium. The net mucosa-to-serosa Na+ transport was enhanced by the addition of bradykinin to the serosal side of the everted intestine, and Na+ transport was further increased by adding bradykinin to the serosal fluid and glucose to the mucosal. The net Na+ transport was suppressed by the addition of ouabain in the serosal fluid, but was restored to the normal level by bradykinin. Measurement of Na+ in the intestine showed that addition of bradykinin to the medium reduced the uptake of Na+ into the tissue and enhanced the efflux of Na+ from the intestine to the medium. Glucose- or valine-evoked transmural potential difference in jejunum segment was elevated by the addition of kallidin to the serosal side, but the transepithelial resistance was not altered. Thus, we suggest that Na+ transport in the small intestine is stimulated by the action of kinins on the serosal side of the intestine, and this acceleration of Na+-flux seems to be accompanied with the enhancement of amino acid and glucose transport.