Bicarbonate Transport Systems in the Intestine of the Seawater EEL

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.