Urotensin-II induces ear flushing in rats

Area of Science:

• Pharmacology
• Physiology
• Cardiovascular Research

Background:

• Urotensin II (U-II) is a potent vasoactive peptide acting at the UT receptor.
• Systemic U-II administration in conscious rats induced observable ear pinna flushing.
• The mechanisms underlying U-II-induced ear flushing required further investigation.

Purpose of the Study:

• To quantify U-II-induced ear flushing in rats by measuring ear pinna temperature changes.
• To explore the potential pharmacological mechanisms responsible for U-II-induced ear flushing.
• To compare the effects of U-II with calcitonin gene-related peptide (CGRP), a known vasodilator.

Main Methods:

• Quantified ear pinna temperature changes following U-II administration.
• Administered pharmacological agents including a UT receptor antagonist (urantide), indomethacin, L-Nomega-nitroarginine methylester (L-NAME), mecamylamine, and propranolol.
• Compared U-II effects to those of CGRP.
• Investigated central nervous system involvement via intracerebroventricular injection.

Main Results:

• U-II (9 microg kg(-1)) induced localized ear flushing with a maximal temperature increase of 9°C and a duration of approximately 30 minutes.
• U-II-induced flushing was blocked by the UT receptor antagonist urantide.
• Indomethacin and L-NAME abolished U-II-induced ear flushing, indicating roles for prostaglandins and nitric oxide.
• CGRP induced a more prolonged flushing response than U-II, unaffected by urantide.
• Central administration of U-II did not mediate the ear flushing response.

Conclusions:

• Urotensin II-induced ear flushing is mediated by peripheral UT receptor activation.
• The vasodilation involved in U-II-induced ear flushing relies on prostaglandins and nitric oxide.
• The central nervous system does not appear to directly mediate this peripheral vascular response to U-II.