Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1986-6-10
pubmed:abstractText
Isoproterenol activates adenylate cyclase indirectly via the beta-receptors. Forskolin, on the other hand, directly activates the adenylate cyclase. Both compounds can induce slow action potentials (APs) in isolated guinea pig papillary muscles, consistent with their ability to activate adenylate cyclase. Acetylcholine (ACh), 1-10 microM, depressed or abolished slow APs induced by isoproterenol or forskolin. There was no difference between the forskolin- and isoproterenol-induced slow APs with regard to their sensitivity to ACh. Similar results were obtained in cultured embryonic chick heart cells. We conclude that forskolin induces slow APs that are essentially the same as those induced by isoproterenol, and that ACh action on depressing slow APs must be either directly on the adenylate cyclase complex and/or on another step entirely (e.g., mediated through increased cGMP.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0746-3898
pubmed:author
pubmed:issnType
Print
pubmed:volume
11
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1-10
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1986
pubmed:articleTitle
Cholinergic attenuation of the electrophysiological effects of forskolin.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.