Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1997-7-1
pubmed:abstractText
The present study was undertaken to examine the effect of dopamine D2 receptor activation on Na+,K(+)-ATPase activity in rat renal proximal tubule suspension. Bromocriptine, a dopamine D2 receptor agonist, produced a concentration (10(-9)-10(-5) M) dependent stimulation of Na+,K(+)-ATPase activity which was antagonized by pretreating the tubules with domperidone (1 microM), a dopamine D2 receptor antagonist. Forskolin (1 microM), a direct activator of adenylyl cyclase, inhibited Na+ K(+)-ATPase activity and reversed the stimulation of Na+,K(+)-ATPase activity induced by bromocriptine. Pertussis toxin (200 ng/ml) treatment also abolished the bromocriptine-induced stimulation of Na+,K(+)-ATPase activity. Bromocriptine attenuated forskolin-stimulated cAMP accumulation which was blocked by pertussis toxin treatment of the tubules. The data suggest that dopamine D2 receptor activation by bromocriptine leads to stimulation of Na+,K(+)-ATPase activity which may be mediated through a pertussis-sensitive G protein and inhibition of adenylyl cyclase in rat renal proximal tubules.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0014-2999
pubmed:author
pubmed:issnType
Print
pubmed:day
26
pubmed:volume
321
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
259-63
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Bromocriptine stimulates Na+, K(+)-ATPase in renal proximal tubules via the cAMP pathway.
pubmed:affiliation
Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, TX 77204-5515, USA.
pubmed:publicationType
Journal Article