Sodium transport in the choroid plexus and salt-sensitive hypertension

Abstract

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 22Na+ 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 22Na+ 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 22Na + was less in sensitive versus resistant rats. High salt did not affect ENaC mRNA or protein, nor the benzamil induced decreases in retained 22Na+ or intracellular [Na+] in either strain. However, high salt increased intracellular [Na+] and attenuated the increase in uptake of 22Na+ 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. © 2009 American Heart Association, Inc.