Utilizing a pH-stat method, the rates of mucosal and serosal alkalinization were measured separately in the seawater eel intestine. These two rates were dependent on contralateral HCO3 concentration and were inhibited by contralateral application of DIDS, an inhibitor of HCO3 transport, indicating that the mucosal and serosal alkalinization are due to HCO3 secretion and absorption, respectively. The mucosal alkalinization was enhanced after inhibiting Na+/K+/Cl cotransport by treatment with bumetanide, furosemide or Ba2+, with a latent period of more than lOmin, suggesting that HCO3 absorption from mucosa to serosa depends on Na+/K+/Cl cotransport. The serosal alkalinization caused by HCO3 absorption was completely abolished after mucosal application of bumetanide. After pretreatment with bumetanide, mucosal omission of Cl halved the enhanced rate of mucosal alkalinization, and Na+ omission had no effect on it; this indicates that the exit of HCO3 into the lumen depends on luminal Cl, i.e. on the existence of the usual C1/HCO3 exchange on the brushborder membrane. When serosal Na+ was removed under the same conditions, mucosal alkalinization was reduced, indicating that HCO3 entry from the serosal fluid depends on Na+. Serosal omission of Cl did not reduce mucosal alkalinization. In addition, serosal alkalinization was enhanced by serosal removal of Na+ but not of Cl. These results suggest that there is a Na+/HCO3 cotransport on the basolateral membrane. A possible model for HCO3 transport systems in the seawater eel intestine is proposed, and a possible role for these transport systems is discussed in relation to Na+, Cl and water transport.

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