{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,20]],"date-time":"2026-01-20T17:20:06Z","timestamp":1768929606573,"version":"3.49.0"},"reference-count":44,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2009,1,29]],"date-time":"2009-01-29T00:00:00Z","timestamp":1233187200000},"content-version":"vor","delay-in-days":728,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2007,2]]},"abstract":"<jats:sec><jats:title>Background and purpose:<\/jats:title><jats:p>While investigating the effects of systemic urotensin II (U\u2010II), 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\u2010II\u2010induced ear flushing was quantified in terms of ear pinna temperature change and potential mechanisms were explored.<\/jats:p><\/jats:sec><jats:sec><jats:title>Experimental approach:<\/jats:title><jats:p>U\u2010II\u2010induced ear flushing was quantified by measuring lateral ear pinna temperature changes and compared to that of calcitonin gene\u2010related peptide (CGRP), a known cutaneous vasodilator. Further, the effects of a variety of pharmacological agents on U\u2010II\u2010induced ear flushing were explored.<\/jats:p><\/jats:sec><jats:sec><jats:title>Key results:<\/jats:title><jats:p>Subcutaneous injection of U\u2010II (9 \u03bcg kg<jats:sup>\u22121<\/jats:sup>)produced localized ear pinna flushing with an onset of \u223c15\u2003min, a duration of \u223c30\u2003min and a maximal temperature change of 9\u00b0C. In contrast, CGRP caused cutaneous flushing within multiple cutaneous beds including the ear pinna with a shorter onset and greater duration than U\u2010II. A potent UT receptor antagonist, urantide, blocked U\u2010II\u2010induced ear flushing but did not affect CGRP\u2010induced ear flushing. Pretreatment with indomethacin or L\u2010N<jats:sup>\n<jats:italic>\u03c9<\/jats:italic><\/jats:sup> \u2010nitroarginine methylester (L\u2010NAME) abolished U\u2010II\u2010induced ear flushing. Mecamylamine or propranolol did not affect this response to U\u2010II. Direct intracerebroventricular injection studies suggested that the ear flushing response to U\u2010II was not mediated directly by the CNS.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion and implications:<\/jats:title><jats:p>Our results suggest that U\u2010II\u2010induced ear flushing and temperature increase is mediated by peripheral activation of the UT receptor and involves prostaglandin\u2010 and nitric oxide\u2010mediated vasodilation of small capillary beds in the rat ear pinna.<\/jats:p><jats:p><jats:italic>British Journal of Pharmacology<\/jats:italic> (2007) <jats:bold>150<\/jats:bold>, 415\u2013423. doi:<jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" 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