Effects of Anoxia and Metabolic Inhibitors on the Sugar-evoked Potential and Demonstration of Sugar-outflow Potential in Toad Intestine

Abstract

The sugar-evoked potential was recorded from everted sacs of the upper segment of toad intestine, and effects on this potential of anoxia, various metabolic inhibitors and ouabain were observed in a lowered external sodium concentratioai. Anoxia of a relatively short duration, KCN plus IAA, and ouabain caused a time-dependent decay of the evoked potential; inhibition of plateau formation, without affecting the imrnediat' potential increment significantly. DNP and prolonged anoxia depressed the size of the immediate increment, but the depression of the plateau was still more prominent. Fluoroacetate, KCN or IAA alone had no effect. Under inhibited conditions, phlorizin, applied at later phases of decaying sugar-evoked potential, produced a potential surge like the mirror-image of the decaying sugar-evoked potential and concurrent increases in sugar and sodium outflows. Similar surge could also be produced by lowering mucosal sugar concentration rapidly at a similar phase. These findings indicate that normal sugar-evoked potential is formed by two distinct mechanisms; relatively metabolism-independent and metabolism-dependent ones, and strongly suggest that the former responsible for the production of the immediate potential increment is directly associated with facilitated diffusion of sodium with sugar molecules on common mobile carriers.