Sodium transport in the choroid plexus and salt-sensitive hypertension.

To elucidate the role of epithelial sodium channels (ENaCs) and Na(+)-K(+)-ATPase in Na(+) transport by the choroid plexus, we studied ENaC expression and Na(+) transport in the choroid plexus. Lateral ventricle choroid plexuses were obtained from young male Wistar, Dahl salt-resistant (SS.BN13), and Dahl salt-sensitive (SS/MCW) rats on a regular (0.3%) or high- (8.0%) salt diet. The effects of ENaC blocker benzamil and Na(+)-K(+)-ATPase blocker ouabain on sodium transport were evaluated by measuring the amounts of retained (22)Na(+) and by evaluating intracellular [Na(+)] with Sodium Green fluorescence. In Wistar rats, ENaC distribution was as follows: microvilli, 10% to 30%; cytoplasm, 60% to 80%; and basolateral membrane, 5% to 10%. Benzamil (10(-8) m) decreased (22)Na(+) retention by 20% and ouabain (10(-3) m) increased retention by 40%, whereas ouabain and benzamil combined caused no change. Similar changes were noted in intracellular [Na(+)]. In Dahl rats on a regular salt diet, intracellular [Na(+)] was similar, but the amount of retained (22)Na(+) was less in sensitive versus resistant rats. High salt did not affect ENaC mRNA or protein, nor the benzamil induced decreases in retained (22)Na(+) or intracellular [Na(+)] in either strain. However, high salt increased intracellular [Na(+)] and attenuated the increase in uptake of (22)Na(+) by ouabain in resistant but not sensitive rats, suggesting a decrease in Na(+)-K(+)-ATPase activity only in resistant rats. These findings suggest that both ENaC and Na(+)-K(+)-ATPase regulate Na(+) transport in the choroid plexus. Aberrant regulation of Na(+) transport and of Na(+)-K(+)-ATPase activity, but not of ENaCs, might contribute to the increase in cerebrospinal fluid [Na(+)] in Dahl salt-sensitive rats on a high-salt diet.