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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions |
umls-concept:C0007452,
umls-concept:C0015127,
umls-concept:C0030685,
umls-concept:C0071163,
umls-concept:C0127400,
umls-concept:C0178719,
umls-concept:C0376604,
umls-concept:C0391871,
umls-concept:C0439831,
umls-concept:C0521428,
umls-concept:C0596235,
umls-concept:C0597484,
umls-concept:C0680255,
umls-concept:C1283071,
umls-concept:C1314792,
umls-concept:C1698986,
umls-concept:C1816453,
umls-concept:C1963578
|
| pubmed:issue |
3
|
| pubmed:dateCreated |
1996-5-14
|
| pubmed:abstractText |
Pituitary adenylate cyclase-activating polypeptide (PACAP) has been reported to increase intracellular Ca2+ concentrations ([Ca2+]i) and catecholamine release in adrenal chromaffin cells. We measured [Ca2+]i with fura-2 and recorded ion currents and membrane potentials with the whole cell configuration of the patch-clamp technique to elucidate the mechanism of PACAP-induced [Ca2+]i increase in bovine adrenal chromaffin cells. PACAP caused [Ca2+]i to increase due to Ca2+ release and Ca2+ influx, and this was accompanied by membrane depolarization and inward currents. The Ca2+ release was suppressed by ryanodine, an inhibitor of caffeine-sensitive Ca2+ stores, but was unaffected by cinnarizine, an inhibitor of inositol trisphosphate-induced Ca2+ release. Ca2+ influx and inward currents were both inhibited by replacement of extracellular Na+, and Ca2+ influx was inhibited by nicardipine, an L-type Ca2+ channel blocker, or by staurosporine, a protein kinase C (PKC) inhibitor, but was unaffected by a combination of omega- conotoxin-GVIA, omega-agatoxin-IVA, and omega-conotoxin- MVIIC, blockers of N-, P-, and Q-type Ca2+ channels. Moreover, 1-oleoyl-2-acetyl-sn-glycerol, a PKC activator, induced inward currents and Ca2+ influx. These results indicate that PACAP causes both Ca2+ release, mainly from caffeine-sensitive Ca2+ stores, and Ca2+ influx via L-type Ca2+ channels activated by membrane depolarization that depends on PKC-mediated Na+ influx.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Mar
|
| pubmed:issn |
0013-7227
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
137
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
956-66
|
| pubmed:dateRevised |
2005-11-17
|
| pubmed:meshHeading |
pubmed-meshheading:8603609-Adrenal Glands,
pubmed-meshheading:8603609-Animals,
pubmed-meshheading:8603609-Biological Transport,
pubmed-meshheading:8603609-Calcium,
pubmed-meshheading:8603609-Cattle,
pubmed-meshheading:8603609-Cells, Cultured,
pubmed-meshheading:8603609-Chromaffin System,
pubmed-meshheading:8603609-Electrophysiology,
pubmed-meshheading:8603609-Membrane Potentials,
pubmed-meshheading:8603609-Neuropeptides,
pubmed-meshheading:8603609-Pituitary Adenylate Cyclase-Activating Polypeptide,
pubmed-meshheading:8603609-Sodium
|
| pubmed:year |
1996
|
| pubmed:articleTitle |
Pituitary adenylate cyclase-activating polypeptide causes rapid Ca2+ release from intracellular stores and long lasting Ca2+ influx mediated by Na+ influx-dependent membrane depolarization in bovine adrenal chromaffin cells.
|
| pubmed:affiliation |
Department of Biomedical Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo, Japan.
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| pubmed:publicationType |
Journal Article
|