title: Therapeutic potential of blockade of the urotensin II system in systemic hypertension.
abstract: Urotensin II, an 11-amino acid peptide, has been found to be the most potent vasoconstrictor yet described, in certain vascular beds. Discovery of its endogenous receptor (UII-R) has ignited considerable interest in this system's role in disease states associated with increased vascular tone (eg, systemic hypertension). Urotensin II was shown to have direct effects on the heart in addition to effects on vascular tone. In human systemic hypertension, increased plasma levels of urotensin II were noted, with a weak but significant correlation to absolute blood pressure levels. Furthermore, hypertensive patients demonstrate net vasoconstrictor responsiveness in skin microcirculation compared to normal controls. Highly selective UII-R antagonists have been developed based on the known structure of UII-R. Early preclinical and clinical studies report potential beneficial effects in renal disease, heart failure, and diabetes, although effects on blood pressure have been equivocal.
authors.affiliation: Department of Epidemiology and Preventive Medicine, Monash University/Alfred Hospital, 89 Commercial Road, Melbourne, VIC 3004, Australia. Henry.Krum@med.monash.edu.au
authors.forename: Henry
authors.initials: H
authors.lastname: Krum
authors.forename: Will
authors.initials: W
authors.lastname: Kemp
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure; D006333:Heart Failure / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000378:metabolism* / Q000503:physiopathology; D007674:Kidney Diseases / Q000378:metabolism / Q000503:physiopathology; D043562:Receptors, G-Protein-Coupled / Q000037:antagonists & inhibitors* / Q000378:metabolism; D014579:Urotensins / Q000187:drug effects / Q000378:metabolism*; D014661:Vasoconstriction
chemical_list: D015415:Biomarkers; D043562:Receptors, G-Protein-Coupled; D014579:Urotensins; C029677:urotensin II