Environmental factors responsible for switching on the SO42−excretory system in the kidney of seawater eels

Author:

Watanabe Taro1,Takei Yoshio1

Affiliation:

1. Laboratory of Physiology, Department of Marine Bioscience, Atmosphere and Ocean Research Institute, The University of Tokyo, Kashiwa, Chiba, Japan

Abstract

Eels are unique in that they maintain lower plasma SO42−concentration in SO42−-rich (∼30 mM) seawater (SW) than in SO42−-poor (<0.3 mM) freshwater (FW), showing drastic changes in SO42−regulation between FW and SW. We previously showed that the expression of renal SO42−transporter genes, FW-specific Slc13a1 and SW-specific Slc26a6a, changes profoundly after transfer of FW eels to SW, which results in the decrease in plasma SO42−concentration after 3 days in SW. In this study, we attempted to identify the environmental factor(s) that trigger the switching of SO42−regulation using changes in plasma and urine SO42−concentrations and expression of the transporter genes as markers. Transfer of FW eels to 30 mM SO42−or transfer of SW eels to SO42−-free SW did not change the SO42−regulation. Major divalent cations in SW, Mg2+(50 mM) and Ca2+(10 mM), were also ineffective, but 50 mM NaCl was effective for switching the SO42−regulation. Further analyses using choline-Cl and Na-gluconate showed that Clis a primary factor and Na+is permissive for the Cleffect. Since plasma SO42−and Clconcentrations were inversely correlated, we injected various solutions into the blood and found that Clalone triggered the switching from FW to SW-type regulation. Furthermore, the inhibitor of Na-Cl cotransporter (NCC) added to media significantly impaired the expression of SW-specific Slc26a6a in 150 mM NaCl. In summary, it appears that Clions in SW are taken up into the circulation via the NCC together with Na+, and the resultant increase in plasma Clconcentration enhances SO42−excretion by the kidney through downregulation of absorptive Slc13a1 and upregulation of excretory Slc26a6a, resulting in low plasma SO42−concentration in SW.

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology

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