Abstract

citrate flux is similar to that found in renal brush border by Wright et al. (1982). The absence of a sodium-independent flux from the renal brush border membrane may implicate the sodium-independent flux component at the basolateral membrane. This proposal for citrate would parallel the hexose and amino acid systems, and would allow net absorption of citrate, which is known to take place (Newsome et al., 1983). We have found that in addition to the sodium dependence of one of the citrate fluxes, citrate significantly increases sodium influx. This increase in sodium influx has been previously seen with both the intestinal hexose and amino acid symport systems (Sepulveda et al., 1982). The pH dependence of citrate influx (Fig. Ib) led us to investigate the possibility that citrate elicits its effects on sodium influx via sodium-proton exchange. We have found a sodium-proton exchange system on the enterocyte membrane and have discovered that this system plays little part in the effects of citrate on sodium influx. We have also found that the citrate-induced increase in sodium influx is unaffected by the sodium-proton exchange inhibitor amiloride. It appears, therefore, that citrate increases the transcellular sodium flux by increasing sodium influx through a symport system. The sodium-independent citrate flux appears to play little part in the increase in sodium flux, and citrate does not indirectly use the sodium-proton exchange system available. Although we have found that the rotenone-poisoned cells do not metabolize citrate over at least 8min, i t has been suggested that citrate acts as a mucosal cell energy source in the dehydrated animal (Bywater, 1977). Therefore, in addition to increasing enterocyte sodium influx, citrate may also elevate depleted ATP pools and sodium ATPase activity, to aid further transcellular sodium flux.

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