Decreases in Systemic Arterial and Hindquarters Perfusion Pressure in Response to Nociceptin Are Not Inhibited by Naloxone in the Rat

Czapla, M. A., H. C. Champion and P. J. Kadowitz. Decreases in systemic arterial and hindquarters perfusion pressure in response to nociceptin are not inhibited by naloxone in the rat. Peptides 18(8) 1197–1200, 1997.—Nociceptin, the endogenous ligand for the ORL 1 receptor, has been shown to decreas...

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Veröffentlicht in:Peptides (New York, N.Y. : 1980) N.Y. : 1980), 1997, Vol.18 (8), p.1197-1200
Hauptverfasser: Czapla, M.A, Champion, H.C, Kadowitz, P.J
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Sprache:eng
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Zusammenfassung:Czapla, M. A., H. C. Champion and P. J. Kadowitz. Decreases in systemic arterial and hindquarters perfusion pressure in response to nociceptin are not inhibited by naloxone in the rat. Peptides 18(8) 1197–1200, 1997.—Nociceptin, the endogenous ligand for the ORL 1 receptor, has been shown to decrease systemic arterial and hindquarters perfusion pressures in the rat. The present study was undertaken to determine if decreases in systemic arterial and hindquarters perfusion pressures, in response to nociceptin, are mediated by a naloxone-sensitive mechanism. Injections of nociceptin decreased systemic arterial and hindquarters perfusion pressures in a dose-related manner. The decreases in systemic arterial and hindquarters perfusion pressure in response to nociceptin were not altered by the administration of naloxone in a dose of 2 mg/kg IV. Met-enkephalin decreased systemic arterial and hindquarters perfusion pressures and responses to the opioid receptor agonist were significantly reduced by naloxone, whereas decreases in systemic arterial pressure in response to the nitric oxide donor, DEA/NO, were not altered. The results of the present study show that decreases in systemic arterial and hindquarters perfusion pressure in response to nociceptin are not mediated by a naloxone-sensitive mechanism in the rat.
ISSN:0196-9781
1873-5169
DOI:10.1016/S0196-9781(97)00178-2