High salt diet down-regulates proximal tubule Na+, K(+)-ATPase activity in Dahl salt-resistant but not in Dahl salt-sensitive rats: evidence of defective dopamine regulation.
We examined the regulation of Na+,K(+)-ATPase activity in proximal tubule segments during a high salt diet in prehypertensive Dahl salt-sensitive and salt-resistant rats. Rats were placed on normal salt or high salt diets (0.9% saline as drinking water). During the normal salt diet, Na+,K(+)-ATPase activity was not different between Dahl salt-sensitive and salt-resistant rats. After 2 days and 10 days on a high salt diet, Na+,K(+)-ATPase activity in Dahl salt-resistant rats significantly decreased when compared to Dahl salt-resistant rats on a normal salt diet (P less than 0.01). The decreased Na+,K(+)-ATPase activity in Dahl salt-resistant rats during a high salt diet was reversed by treatment with an inhibitor of aromatic L-amino acid decarboxylase (dopamine synthesizing enzyme), benserazide. In contrast, Na+,K(+)-ATPase activity did not decrease during the high salt diet and benserazide had no effect on Na+,K(+)-ATPase activity in Dahl salt-sensitive rats. These results indicate that Dahl salt-sensitive rats do not have the capacity to down-regulate the proximal tubule Na+,K(+)-ATPase activity during a high salt diet. Indirect evidence suggests that the regulation of Na+,K(+)-ATPase activity by locally produced dopamine is absent in Dahl salt-sensitive rats.
Nishi
A
A
Department of Paediatrics, Karolinska Institute, Sweden.
Bertorello
A M
AM
Aperia
A
A
D000818:Animals; D004298:Dopamine / Q000378:metabolism; D015536:Down-Regulation; D006973:Hypertension / Q000209:etiology* / Q000378:metabolism; D007687:Kidney Tubules, Proximal / Q000201:enzymology*; D008297:Male; D051381:Rats; D012982:Sodium, Dietary / Q000008:administration & dosage*; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*
D012982:Sodium, Dietary; D000254:Sodium-Potassium-Exchanging ATPase; D004298:Dopamine