Linked Life Data

2821231

Source:http://linkedlifedata.com/resource/pubmed/id/2821231

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1987-11-5
pubmed:abstractText
To determine the role of activated protein kinase C in vascular smooth muscle contraction, phorbol dibutyrate was used to stimulate this enzyme in order to evaluate the source(s) of Ca++ (10(-8) to 3 X 10(-6) M) elicited a concentration-dependent sustained contraction which was slow in onset but progressive in developed tension. The maximal contractile response induced by phorbol dibutyrate was only partly dependent on influx of extracellular Ca++ as shown by similar reductions (40%) produced by Ca++-free buffer, LaCl3 (1 mM) or nifedipine (10(-6) M). These data suggest that phorbol dibutyrate is able to open Ca++ channels which are sensitive to nifedipine blockade. However, unlike norepinephrine or K+-depolarization, phorbol dibutyrate evoked a slow 45Ca++ influx which occurred only after extended contact time. Pretreatment with nifedipine again abolished this response. In contrast to norepinephrine, phorbol dibutyrate did not cause 45Ca++ efflux indicating that intracellular Ca++ was not mobilized. It is concluded that the residual 60% contraction to phorbol dibutyrate most likely occurs via a mechanism independent of the Ca-calmodulin pathway.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0022-3565
pubmed:author
pubmed:issnType
Print
pubmed:volume
242
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
934-9
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1987
pubmed:articleTitle
Ca++ utilization in the constriction of rat aorta to stimulation of protein kinase C by phorbol dibutyrate.
pubmed:affiliation
E. I. du Pont de Nemours and Company, Inc., Medical Products Department, Wilmington, Delaware.
pubmed:publicationType
Journal Article, In Vitro