Linked Life Data

10499871

Source:http://linkedlifedata.com/resource/pubmed/id/10499871

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
1999-10-14
pubmed:abstractText
Steroid hormones exert their biological actions via intracellular receptors modulation of transcription. In addition, a number of molecular interactions, and the existence of membrane receptors in several tissues, support the hypothesis of nongenomic action of steroids. The androgens, 5alpha- and 5beta-dihydrotestosterone (0.1 to 100 microM), induce a rapid positive inotropism in the isolated left atrium of male Wistar rats whose time course of response might suggest that it is a non-genomic effect. However, the fact that the facilitation of contractility was inhibited by actinomycin D (5 microg/ml) and cycloheximide (10 microg/ml) indicates that a transcriptional component might play a role. The existence of a rapid functional genomic role would be somewhat surprising. However, rapid transcriptional mechanisms were also observed in certain cAMP-dependent responses. In the left atrium of rat, Rp-cAMPS (10 microM), a cAMP-dependent protein kinase inhibitor, antagonized 5alpha- but not 5beta-dihydrotestosterone-induced positive inotropism. The inhibition by Rp-cAMPS of isoproterenol- and forskolin-induced positive inotropism, and the fact that these cAMP-dependent effects were also inhibited by actinomycin D and cycloheximide, suggest that a cAMP-dependent transcriptional component may be partly involved in the positive inotropism induced by 5alpha-dihydrotestosterone. In addition, 5alpha-dihydrotestosterone might increase the basal adenylyl cyclase activity by acting on unoccupied beta-adrenoceptor-G-protein-adenylyl cyclase complexes, since the elicited inotropism was inhibited by a beta-blocker, atenolol (1 microM), a G-protein inhibitor, pertussis toxin (2 microg/ml, 3 h), and an adenylyl cyclase inhibitor, dideoxy-adenosine (10 microM).
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0024-3205
pubmed:author
pubmed:issnType
Print
pubmed:volume
65
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1035-45
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:10499871-Adenylate Cyclase Toxin, pubmed-meshheading:10499871-Animals, pubmed-meshheading:10499871-Atenolol, pubmed-meshheading:10499871-Cyclic AMP, pubmed-meshheading:10499871-Cycloheximide, pubmed-meshheading:10499871-Dactinomycin, pubmed-meshheading:10499871-Dideoxyadenosine, pubmed-meshheading:10499871-Dihydrotestosterone, pubmed-meshheading:10499871-Electric Stimulation, pubmed-meshheading:10499871-Gene Expression, pubmed-meshheading:10499871-Heart Atria, pubmed-meshheading:10499871-Isoproterenol, pubmed-meshheading:10499871-Male, pubmed-meshheading:10499871-Myocardial Contraction, pubmed-meshheading:10499871-Pertussis Toxin, pubmed-meshheading:10499871-Rats, pubmed-meshheading:10499871-Rats, Wistar, pubmed-meshheading:10499871-Reserpine, pubmed-meshheading:10499871-Stimulation, Chemical, pubmed-meshheading:10499871-Virulence Factors, Bordetella
pubmed:year
1999
pubmed:articleTitle
Positive inotropism induced by androgens in isolated left atrium of rat: evidence for a cAMP-dependent transcriptional mechanism.
pubmed:affiliation
Servicio de Cardiología, Hospital Central Asturias, Oviedo, Spain.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't