Chronic treatment with nifedipine prevents development of hypertension and abnormal red cell Na+ transport in Dahl-S-rats.
Transmembrane Na+ transport was measured in erythrocytes of salt resistant (DR) and salt sensitive (DS) Dahl rats, fed either a standard (0.4%) or high (0.8%) NaCl diet, or a high NaCl diet containing 300 ppm of the calcium entry blocker nifedipine. Whereas salt-loaded DS became severely hypertensive, those treated with nifedipine remained normotensive. With a low NaCl diet, total Na+ efflux and Na+ pump activity was lower in DS than in DR. Cotransport was more active in DS than in DR. After excess Na+ intake, total Na+ efflux was markedly reduced in DS, but normal in nifedipine-treated DS. Cell Na+ content was increased by 52% in salt-loaded DS, but not so in DS chronically treated with nifedipine. Na+ pump was completely suppressed in salt-loaded DS, but normal in DR and rats treated with nifedipine. These results suggest that Na+ pump inhibition might be involved in the development of Dahl rat hypertension, and that prevention of salt-induced hypertension by chronic nifedipine treatment also prevents suppression of erythrocytic Na+ pump. This suggests a casual link between its biochemical and therapeutic action.
A
A
Knorr
M
M
De Mendonça
B
B
Garthoff
F
F
Morich
S
S
Kazda
D000818:Animals; D002034:Bumetanide / Q000494:pharmacology; D004910:Erythrocyte Membrane / Q000378:metabolism; D004912:Erythrocytes / Q000187:drug effects / Q000378:metabolism*; D005260:Female; D006973:Hypertension / Q000097:blood* / Q000517:prevention & control; D066298:In Vitro Techniques; D007473:Ion Channels / Q000187:drug effects; D008274:Magnesium / Q000494:pharmacology; D015636:Magnesium Chloride; D009543:Nifedipine / Q000494:pharmacology*; D010042:Ouabain / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000097:blood*
D007473:Ion Channels; D015636:Magnesium Chloride; D002034:Bumetanide; D010042:Ouabain; D012964:Sodium; D008274:Magnesium; D009543:Nifedipine