Article date: February 2007
By: J‐S Qi, R Schulingkamp, T J Parry, R Colburn, D Stone, B Haertlein, L K Minor, P Andrade‐Gordon, B P Damiano in Volume 150, Issue 4, pages 415-423
Background and purpose:
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.
Experimental approach:
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.
Key results:
Subcutaneous injection of U‐II (9 μg kg−1)produced localized ear pinna flushing with an onset of ∼15 min, a duration of ∼30 min and a maximal temperature change of 9°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‐Nω ‐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.
Conclusion and implications:
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.
DOI: 10.1038/sj.bjp.0707006
View this article