Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1997-1-17
pubmed:abstractText
Since duodenal bicarbonate secretion (DBS) is increased by m-cholinoceptor agonists, it was postulated that protein kinase C (PKC) has a role in this secretion. This premise was examined in guinea pigs, using 12-O-tetradecanoyl-phorbol 13-acetate (TPA) to stimulate bicarbonate production in the perfused duodenum in vivo, and to activate PKC in isolated duodenal enterocytes. TPA (10(-7) mol.kg-1) infused intravenously stimulated active DBS from basal values of 3.64 +/- 0.66 to 8.73 +/- 1.59 mumol.cm-1.10 min-1. This effect was completely blocked by verapamil (4 x 10(-7) mol.kg-1). PKC activity in duodenal enterocytes in the basal state was most abundant in the cytosolic fraction (2,221 +/- 444 U/mg protein) and very low in the particulate fraction (227 +/- 51 U/mg protein). TPA (10(-7) mol.kg-1) caused a time-dependent translocation of the cytosolic, lipid-dependent activity of PKC into the particulate fraction. The effect was maximal at 5 min incubation and was reversed by 30 min. In the particulate fraction, this activity was no longer lipid-dependent, but could be stimulated by Ca2+ alone. These data support the hypothesis that translocation of PKC may contribute to DBS.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0031-7012
pubmed:author
pubmed:issnType
Print
pubmed:volume
53
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
60-5
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Role of protein kinase C in duodenal mucosal bicarbonate secretion in the guinea pig.
pubmed:affiliation
Gastroenterology Institute, Soroka Medical Center, Beer Sheva, Israel.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't