Urotensin-II induces ear flushing in rats
| Autor: | J-s, Qi, R, Schulingkamp, T J, Parry, R, Colburn, D, Stone, B, Haertlein, L K, Minor, P, Andrade-Gordon, B P, Damiano |
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| Rok vydání: | 2007 |
| Předmět: |
Male
Nitric Oxide Synthase Type III Calcitonin Gene-Related Peptide Injections Subcutaneous Urotensins Vasodilator Agents Adrenergic beta-Antagonists Anti-Inflammatory Agents Non-Steroidal Indomethacin Nicotinic Antagonists Mecamylamine Propranolol Research Papers Body Temperature Rats Rats Sprague-Dawley NG-Nitroarginine Methyl Ester Regional Blood Flow Flushing Animals Ear External Enzyme Inhibitors |
| Zdroj: | British journal of pharmacology. 150(4) |
| ISSN: | 0007-1188 |
| Popis: | While investigating the effects of systemic urotensin II (U-II), a potent vasoactive peptide acting at the UT receptor, we observed ear pinna flushing after systemic administration to conscious rats. In the present study, U-II-induced ear flushing was quantified in terms of ear pinna temperature change and potential mechanisms were explored.U-II-induced ear flushing was quantified by measuring lateral ear pinna temperature changes and compared to that of calcitonin gene-related peptide (CGRP), a known cutaneous vasodilator. Further, the effects of a variety of pharmacological agents on U-II-induced ear flushing were explored.Subcutaneous injection of U-II (9 microg kg(-1))produced localized ear pinna flushing with an onset of approximately 15 min, a duration of approximately 30 min and a maximal temperature change of 9 degrees C. In contrast, CGRP caused cutaneous flushing within multiple cutaneous beds including the ear pinna with a shorter onset and greater duration than U-II. A potent UT receptor antagonist, urantide, blocked U-II-induced ear flushing but did not affect CGRP-induced ear flushing. Pretreatment with indomethacin or L-Nomega-nitroarginine methylester (L-NAME) abolished U-II-induced ear flushing. Mecamylamine or propranolol did not affect this response to U-II. Direct intracerebroventricular injection studies suggested that the ear flushing response to U-II was not mediated directly by the CNS.Our results suggest that U-II-induced ear flushing and temperature increase is mediated by peripheral activation of the UT receptor and involves prostaglandin- and nitric oxide-mediated vasodilation of small capillary beds in the rat ear pinna. |
| Databáze: | OpenAIRE |
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