Bicarbonate Transport Systems in the Intestine of the Seawater EEL

Abstract

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.