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

Abstract

Nishi, A., Bertorello, A. M. & Aperia, A. 1992. 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. Acta Ptiysiol Scand144, 263–267. Received 26 July 1991, accepted 25 October 1991. ISSN 0001–6772. Department of Paediatrics, Karolinska Institute, SwedenWe 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 < 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.