William Kemp, Stuart Roberts and Henry Krum Pages 159 - 168 ( 10 )
Urotensin II is the most potent vasoconstrictor known. Paradoxically, urotensin II also possesses vasodilator activity in certain vascular beds. While much is still to be learnt regarding urotensin IIs actions on vascular tone, it is now clear that it mediates its effects by interacting with a specific G-protein-coupled receptor. The presence of urotensin II and its receptor in both vertebrate and invertebrate species suggests an evolutionarily conserved role in normal physiology although evidence is mounting for both species-specific as well as disease-specific effects of this peptide. This somatostatin- like peptide was originally thought to reside solely in compartments of the central nervous system. However, recent evidence implicated urotensin II in the pathogenesis of a variety of disease processes ranging from hypertension to hepatic cirrhosis. Increased expression of this peptide has been noted in cardiac, renal and hepatic disease. While the contribution of urotensin II to these diseases remains unclear, the advent of urotensin II antagonists allows for not only the possibility of a new range of therapeutic drugs but also new avenues of investigation and further mechanistic insights into the pathophysiology of these disease processes.
neurosecretory system, urophysis, chromosome, vasoconstriction, somatostatin receptor, cardiac failure, hypertension, atherosclerosis, angiotensin II
Director NHMRC CCRE Therapeutics, Department of Epidemiology&Preventive Medicine and Department of Medicine Monash University, Faculty of Medicine, Nursing and Health Sciences, The Alfred, Commercial Road, Melbourne, VIC 3004, Australia.