| Nociceptin/orphanin FQ alters prostaglandin cerebrovascular action following brain injury. | |
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MedLine Citation:
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PMID: 15000759 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Previous studies have observed that fluid percussion brain injury (FPI) elevated the CSF concentration of the opioid nociceptin/orphanin FQ (NOC/oFQ). In separate studies, FPI impaired pial artery dilation to the prostaglandins PGI2 and PGE2. This study was designed to investigate the following: (1) role of NOC/oFQ in impaired dilation to PGI2 and PGE2, (2) the effects of FPI on vasoconstriction to the TXA2 mimic U46619 and PGF2alpha, and (3) the role of NOC/oFQ in such FPI induced effects on U46619 and PGF(2alpha). Lateral FPI was induced in newborn pigs equipped with a closed cranial window. PGI2 (1, 10, 100 ng/ml) vasodilation was blunted by FPI and fully restored by the NOC/oFQ antagonist, [F/G] NOC/oFQ (1-13) NH2 (10(-6)M) (9 +/- 1, 13 +/- 1, and 19 +/- 1 vs. 2 +/- 1, 4 +/- 1, and 5 + 1 vs 7 +/- 1, 12 +/- 2, and 17 +/- 3% for control, FPI, and FPI + [F/G] NOC/oFQ (1-13) NH2, respectively). Similar effects were observed for PGE2. In contrast, U46619 (1, 10 ng/ml) induced vasoconstriction was potentiated by FPI but returned to the response observed prior to FPI by [F/G] NOC/oFQ (1-13) NH2 ( -8 +/- 1 and -14 +/- 1 vs. -15 +/- 1 and -25 +/- 1 vs. -7 +/- 1 and -12 +/- 2% for control, FPI, and FPI + [F/G] NOC/oFQ (1-13) NH2, respectively). Similar effects were observed for PGF(2alpha). Coadministration of NOC/oFQ (10(-10)M), the CSF concentration observed after FPI, with agonists under nonbrain injury conditions blunted PGI2 and PGE2 vasodilation, but potentiated U46619 and PGF2alpha vasoconstriction similarly to that observed after FPI. These data show that FPI blunted PGI2 and PGE2 vasodilation but potentiated U46619 and PGF2alpha vasoconstriction. Additionally, these data show that administration of a NOC/oFQ receptor antagonist prevented such FPI associated events. NOC/oFQ administrated in a concentration observed after FPI produced blunted dilator prostaglandin and potentiated vasoconstriction prostaglandin vascular responses under nonbrain injury conditions. Finally, these data suggest that NOC/oFQ alters prostaglandin cerebrovascular action following brain injury. |
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Authors:
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Jonathan Ford; William M Armstead |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Journal of neurotrauma Volume: 21 ISSN: 0897-7151 ISO Abbreviation: J. Neurotrauma Publication Date: 2004 Feb |
Date Detail:
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Created Date: 2004-03-05 Completed Date: 2004-04-12 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 8811626 Medline TA: J Neurotrauma Country: United States |
Other Details:
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Languages: eng Pagination: 187-93 Citation Subset: IM |
Affiliation:
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Departments of Anesthesia and Pharmacology, University of Pennsylvania, Philadelphia, Pennsylvania, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid
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pharmacology Animals Animals, Newborn Blood Chemical Analysis Blood Pressure Brain Injuries / metabolism* Cerebrovascular Circulation / drug effects, physiology Dinoprostone / pharmacology* Epoprostenol / pharmacology* Female Male Opioid Peptides / metabolism* Swine Vasoconstrictor Agents / pharmacology |
| Chemical | |
Reg. No./Substance:
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0/Opioid Peptides; 0/Vasoconstrictor Agents; 0/nociceptin; 35121-78-9/Epoprostenol; 363-24-6/Dinoprostone; 76898-47-0/15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid |
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