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Contractile responses to rat urotensin II in resting and depolarized basilar arteries
Authors:Cristina Porras-González  Juan Ureña  Juan José Egea-Guerrero  Elena Gordillo-Escobar  Francisco Murillo-Cabezas  María del Carmen González-Montelongo  María Ángeles Muñoz-Sánchez
Institution:1. Instituto de Biomedicina de Sevilla and Departamento de Fisiología Médica y Biofísica, Hospital Universitario Virgen del Rocío/CSIC/Universidad de Sevilla, Avenida Manuel Siurot s/n, 41013, Seville, Spain
2. Unidad de Gestión Clínica de Cuidados Críticos y Urgencias, Hospital Universitario Virgen del Rocío, IBIS/CSIC/Universidad de Sevilla, Avenida Manuel Siurot s/n, 41013, Seville, Spain
3. Departamento de Medicina, Universidad de Sevilla, Avenida Sánchez Pizjuan, no. 4, 41009, Seville, Spain
Abstract:The effects of human urotensin II (hUII) on the vascular tone of different animal species has been studied extensively. However, little has been reported on the vasoactive effects of rat urotensin (rUII) in murine models. The aim of the present study was to investigate the effects of rUII on vasoreactivity in rat basilar arteries. Basilar arteries from adult male Wistar rats (300–350 g) were isolated, cut in rings, and mounted on a small vessel myograph to measure isometric tension. rUII concentrations were studied in both resting and depolarized state. To remove endothelial nitric oxide effects from the rUII response, we treated selected arterial rings with Nω-nitro-L-arginine methyl ester (L-NAME). 10 μM rUII produced a potent vasoconstrictor response in rat basilar arteries with intact endothelium, while isometric forces remained unaffected in arterial rings treated with lower rUII concentrations. Although L-NAME did not have a significant effect on 10 μM rUII-evoked contraction, it slightly increased arterial ring contraction elicited by 1 μM rUII. In depolarized arteries, dose-dependent rUII increased depolarization-induced contractions. This effect was suppressed by L-NAME. Our results show that the rat basilar artery has a vasoconstrictor response to rUII. The most potent vasoconstrictor effect was produced by lower doses of rUII (0.1 and 1 μM) in depolarized arteries with intact endothelium. This effect could facilitate arterial vasospasm in vascular pathophysiological processes such as subarachnoid hemorrhage and hypertension, when sustained depolarization and L-type Ca2+ channel activation are present.
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