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Hypertension, Vol 21, 364-372, Copyright © 1993 by American Heart Association
C Chen, RE Beach and MF Lokhandwala
We have previously reported that dopamine-1 receptor-mediated activation of
phospholipase C is diminished in renal cortical slices of adult
spontaneously hypertensive rats. To determine the potential consequences of
this phenomenon, we performed the present studies in which renal proximal
tubule suspensions obtained from spontaneously hypertensive and
Wistar-Kyoto rats of 10-12 weeks of age were used. The tubule suspensions
were incubated with dopamine in the presence or absence of dopamine
receptor antagonists, and sodium, potassium adenosine trisphosphatase
(sodium pump) activity was measured as the ouabain-sensitive adenosine
trisphosphate hydrolysis. We found that dopamine produced a
concentration-related inhibition of sodium pump activity in the
normotensive rats but not in the hypertensive rats. Dopamine-induced
inhibition of sodium pump activity in the normotensive rats was abolished
by the phospholipase C inhibitor U-73122 or the protein kinase C inhibitor
sphingosine, suggesting the involvement of a phospholipase C-coupled
protein kinase C pathway in this response. Dopamine-induced inhibition in
the normotensive rats was attenuated by the dopamine-1 receptor antagonist
SCH 23390 but not by the dopamine-2 receptor antagonist domperidone. To
identify possible sites of defect in dopamine-1 receptor-coupled signaling
pathways in the hypertensive rats, we incubated the proximal tubules with
phorbol 12,13-dibutyrate or the synthetic diacylglycerol analogue
1-oleoyl-2-acetyl-rac- glycerol. The results showed that both compounds
inhibited sodium pump activity as effectively in the hypertensive as in the
normotensive rats, suggesting that the protein kinase C-coupled sodium pump
pathway was not defective in the hypertensive animals.(ABSTRACT TRUNCATED
AT 250 WORDS)
ARTICLES
Dopamine fails to inhibit renal tubular sodium pump in hypertensive rats
Department of Pharmacology, University of Houston, TX 77204-5515.
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