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(Hypertension. 2009;54:860.)
© 2009 American Heart Association, Inc.

Original Articles

Sodium Transport in the Choroid Plexus and Salt-Sensitive Hypertension

Md Shahrier Amin; Erona Reza; Hongwei Wang; Frans H.H. Leenen

From the Hypertension Unit (M.S.A., E.R., H.W., F.H.H.L.), University of Ottawa Heart Institute, Ottawa, Ontario, Canada; Department of Cellular and Molecular Medicine (M.S.A., E.R., F.H.H.L.), University of Ottawa, Ottawa, Ontario, Canada.

Correspondence to Frans H.H. Leenen, Hypertension Unit, University of Ottawa Heart Institute, 40 Ruskin St, Room H-3238, Ottawa, Ontario K1Y4W7, Canada. E-mail fleenen{at}ottawaheart.ca

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.

Key Words: sodium • choroid plexus • ENaC • Na⁺-K⁺-ATPase • Dahl rats • hypertension