Linked Life Data

9117386

Source:http://linkedlifedata.com/resource/pubmed/id/9117386

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
1997-4-22
pubmed:abstractText
The effects of arachidonic acid (AA) and arachidonic acid metabolites on vasopressin secretion and on intracellular free calcium concentration ([Ca2+]i) from both intact and streptolysin-O permeabilized isolated nerve endings of the rat neurohypophysis were studied. Arachidonic acid induced a dose-dependent increase in resting vasopressin (AVP) secretion in both intact and streptolysin-O permeabilized nerve endings. Although AA also dose-dependently induced an increase in [Ca2+]i in intact nerve endings, the AA-induced secretory response was largely independent of an increase in [Ca2+]i. Secretory responses in intact nerve endings showed AA-induced secretion to be sustained and that AA-induced vasopressin secretion occurs via exocytosis. Arachidonic acid also dose-dependently potentiated K+-depolarization evoked vasopressin release. The potentiation of secretion occurred despite an AA-induced reduction in K+-evoked Ca2+ influx. In addition, AA reinitiated secretion following a decline in the Ca2+-dependent exocytotic secretory response suggesting a separate secretory mechanism from Ca2+-induced secretion. Inhibition of the metabolic pathways for AA suggested that AA itself mediates the secretory effects and that AA is likely subject to rapid metabolism by lipoxygenases.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
2
pubmed:volume
742
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
129-40
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Arachidonic acid regulation of vasopressin release and intracellular Ca2+ in neurohypophysial nerve endings.
pubmed:affiliation
Department of Physiology, University of Michigan, Ann Arbor 48109, USA. esterm@umich.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't