Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2000-5-9
pubmed:abstractText
D1-selective dopamine receptor agonists inhibit secretagogue-stimulated catecholamine secretion from bovine adrenal chromaffin cells. The purpose of the studies reported here was to use the radiolabeled D1-selective dopamine receptor antagonist, SCH23390, to characterize putative D1-like dopamine receptors responsible for this effect. Characterization of SCH23390 binding sites demonstrated an unusual pharmacological profile inconsistent with classical D1-like receptors. [125I]SCH23390 bound to adrenal medullary membranes was competed for by nonradioactive iodo-SCH23390 (Kd = 490 +/- 50 nM), but not by (+)butaclamol. Other classical D1 antagonists had little, if any, effect. Competition with dopamine receptor agonists demonstrated a relative rank order of potency profile characteristic of D1-like dopamine receptors, however, K(i)s were higher than those found in other tissues. The K(i)s for competition of [125I]SCH23390 binding by Cl-APB and SKF38393 (16 and 118 microM, respectively) are nearly identical to the IC(50)s previously observed for inhibition of secretion (9 and 100 microM, respectively). Combined these data suggest that adrenal medullary membranes contain a novel SCH23390 binding site involved in the inhibition of secretion by D1-selective agonists.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0364-3190
pubmed:author
pubmed:issnType
Print
pubmed:volume
25
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
321-6
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Atypical SCH23390 binding sites are present on bovine adrenal medullary membranes.
pubmed:affiliation
Department of Biochemistry, College of Medicine, University of Tennessee, Memphis 38163, USA. mdahmer@utmem1.utmem.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.