Endothelin-1 and angiotensin-II modulate urotensin-II vasoconstriction in rat aorta exposed to mercury

Abstract

Objectives: The aim of this study was to evaluate the possible roles of endothelin-1 and angiotensin-II in urotensin-II vasoconstriction and in endothelial dysfunction induced by mercury.

Background: Urotensin-II, the most potent vasoactive peptide, is entwined with the cardiovascular diseases and has been labelled as a new pathophysiological biomarker.

Methods: Rat aortic rings were pre-incubated with sb-710411, bq-123, and captopril. Doses of human urotensin-II with increased concentrations were applied in all groups in the presence or absence of mercury chloride. In another set of the experiment, aortic rings were treated with a single dose of mercury chloride in the presence of each of the above blockers.

Results: Angiotensin-II and endothelin-1 mediated the vascular responses to the peptide urotensin-II under conditions of both intact endothelium and endothelial impairments induced by mercury. Urotensin-II, angiotensin-II and endothelin-1 significantly participated in vascular responses to mercury chloride.

Conclusion: The novel finding was that urotensin-II is potentiated under the condition of endothelial dysfunction. Endothelin-1 and angiotensin-II pathways could be heavily exploited in modulating endothelial dysfunction impacts and peptide vascular actions (Tab. 1, Fig. 4, Ref. 30).

Keywords: angiotensin-II; endothelial dysfunction; endothelin-1 mercury chloride.; urotensin-II.