title: 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 (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.
authors.affiliation: Hypertension Unit, University of Ottawa Heart Institute, 40 Ruskin Street, Ottawa, Ontario, Canada.
authors.forename: Md Shahrier
authors.initials: MS
authors.lastname: Amin
authors.forename: Erona
authors.initials: E
authors.lastname: Reza
authors.forename: Hongwei
authors.initials: H
authors.lastname: Wang
authors.forename: Frans H H
authors.initials: FH
authors.lastname: Leenen
mesh_terms: D000584:Amiloride / Q000031:analogs & derivatives / Q000494:pharmacology; D000818:Animals; D001692:Biological Transport / Q000187:drug effects / Q000502:physiology; D002831:Choroid Plexus / Q000187:drug effects / Q000378:metabolism*; D004195:Disease Models, Animal; D062686:Epithelial Sodium Channel Blockers; D053503:Epithelial Sodium Channels / Q000378:metabolism; D006973:Hypertension / Q000378:metabolism*; D008297:Male; D010042:Ouabain / Q000494:pharmacology; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D020303:Rats, Inbred Dahl; D017208:Rats, Wistar; D012964:Sodium / Q000134:cerebrospinal fluid / Q000378:metabolism*; D012982:Sodium, Dietary / Q000494:pharmacology; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors / Q000378:metabolism
chemical_list: D062686:Epithelial Sodium Channel Blockers; D053503:Epithelial Sodium Channels; D012333:RNA, Messenger; D012982:Sodium, Dietary; C013407:benzamil; D010042:Ouabain; D000584:Amiloride; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase