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Effects of urotensin II on hypoxia‐induced ANP secretion in rats

Urotensin II (UII) is a vasoactive peptide with many potent effects in the cardiovascular system through a G‐protein‐coupled receptor termed UT. The synthesis and secretion of atrial natriuretic peptide (ANP) are increased during hypoxic condition and plays an important role in adaptation to hypoxia and in the pathogenesis of cardiopulmonary diseases. The present study was to investigate the effects of human UII (hUII) on ANP secretion in hypoxia condition in vitro and in vivo experiments. Hypoxia caused an increase in ANP secretion compared to normoxia in isolated perfused beating rat atria. hUII (10‐10 M) decreased hypoxia‐induced ANP secretion whereas hUII receptor antagonist, urantide (10‐6 M), increased it. However, there were no significant changes in atrial contractility, stroke volume, and extracellular fluid (ECF) translocation by hUII in hypoxia condition. The pretreatment with urantide attenuated the effect of hUII on hypoxia‐induced ANP secretion. Monocrotaline‐treated (MCT, 60mg/kg, sc., 4weeks) rats increased UII level in plasma. In vivo experiment, hUII (5*10‐6 M injection plus 2.5*10‐6 M infusion for 15 min) was infused into MCT‐treated and control rats anesthetized with ketamine. hUII increased blood pressure and heart rate in both groups without significant difference. Interestingly, intravenous infusion of hUII decreased plasma concentration of ANP in MCT‐treated rats whereas hUII increased plasma concentration of ANP in control rats. The ANP generation may protect against the hypoxia and pulmonary hypertension. These results suggest that hUII may play a pathophysiological role in the regulation of ANP secretion in hypoxic condition. Supported by the KOSEF (R13‐2008‐005‐00000‐0).