| http://purl.uniprot.org/citations/10670413 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/10670413 | http://www.w3.org/2000/01/rdf-schema#comment | "The modulation of high-voltage-activated (HVA) Ca2+ channels by the prostaglandin E series (PGE1 and PGE2) was studied in the paratracheal ganglion cells. Prostaglandin E1, E2, STA2 (a stable analogue of thromboxane A2), 17-phenyl-trinor-PGE2 (an EP1-selective agonist) and sulprostone (an EP3-selective agonist) inhibited the HVA Ca2+ current (HVA ICa) dose-dependently, and the rank order of potency to inhibit HVA Ca2+ channels was sulprostone>PGE2, PGE1>STA2>>17-phenyl-trinor-PGE2. SC-51089 (10(-5) M), a selective EP1-receptor antagonist, showed no effect on the PGE1- or PGE2-induced inhibition of the HVA ICa, thereby indicating that PGE1- and PGE2-induced inhibition of the HVA Ca2+ channels is possibly mediated by the EP3 receptor. The PGE1-sensitive component of the current was markedly reduced in the presence of omega-conotoxin-GVIA (3x10(-6) M), but not with nifedipine (3x10(-6) M). PGE1 and PGE2 also inhibited the remaining ICa in a saturating concentration of nifedipine, omega-conotoxin-GVIA and omega-conotoxin-MVIIC, suggesting that R-type Ca2+ channels are involved. The inhibitory effect of PGE1 or sulprostone was prevented by pretreatment with pertussis toxin [islet activating protein (IAP)] or phorbol-12-myristate-13-acetate (PMA), and the protein kinase C (PKC) inhibitor chelerythrine blocked the action of PMA. It was concluded that PGE1 selectively reduces both N- and R-type Ca2+ currents by activating a G-protein probably through the EP3 receptor in paratracheal ganglion cells."xsd:string |
| http://purl.uniprot.org/citations/10670413 | http://purl.org/dc/terms/identifier | "doi:10.1016/s0028-3908(99)00142-2"xsd:string |
| http://purl.uniprot.org/citations/10670413 | http://purl.uniprot.org/core/author | "Ito Y."xsd:string |
| http://purl.uniprot.org/citations/10670413 | http://purl.uniprot.org/core/author | "Ishibashi H."xsd:string |
| http://purl.uniprot.org/citations/10670413 | http://purl.uniprot.org/core/author | "Murai Y."xsd:string |
| http://purl.uniprot.org/citations/10670413 | http://purl.uniprot.org/core/author | "Akaike N."xsd:string |
| http://purl.uniprot.org/citations/10670413 | http://purl.uniprot.org/core/author | "Onoue H."xsd:string |
| http://purl.uniprot.org/citations/10670413 | http://purl.uniprot.org/core/date | "2000"xsd:gYear |
| http://purl.uniprot.org/citations/10670413 | http://purl.uniprot.org/core/name | "Neuropharmacology"xsd:string |
| http://purl.uniprot.org/citations/10670413 | http://purl.uniprot.org/core/pages | "181-190"xsd:string |
| http://purl.uniprot.org/citations/10670413 | http://purl.uniprot.org/core/title | "The prostaglandin E series modulates high-voltage-activated calcium channels probably through the EP3 receptor in rat paratracheal ganglia."xsd:string |
| http://purl.uniprot.org/citations/10670413 | http://purl.uniprot.org/core/volume | "39"xsd:string |
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