title: Elevated plasma levels of human urotensin-II immunoreactivity in congestive heart failure.
abstract: Human urotensin-II (hU-II) is the most potent endogenous cardiostimulant identified to date. We therefore determined whether hU-II has a possible pathological role by investigating its levels in patients with congestive heart failure (CHF). Blood samples were obtained from the aortic root, femoral artery, femoral vein, and pulmonary artery from CHF patients undergoing cardiac catheterization and the aortic root from patients undergoing investigative angiography for chest pain who were not in heart failure. Immunoreactive hU-II (hU-II-ir) levels were determined with radioimmunoassay. hU-II-ir was elevated in the aortic root of CHF patients (230.9 +/- 68.7 pg/ml, n = 21; P < 0.001) vs. patients with nonfailing hearts (22.7 +/- 6.1 pg/ml, n = 18). This increase was attributed to cardiopulmonary production of hU-II-ir because levels were lower in the pulmonary artery (38.2 +/- 6.1 pg/ml, n = 21; P < 0.001) than in the aortic root. hU-II-ir was elevated in the aortic root of CHF patients with nonischemic cardiomyopathy (142.1 +/- 51.5 pg/ml, n = 10; P < 0.05) vs. patients with nonfailing hearts without coronary artery disease (27.3 +/- 12.4 pg/ml, n = 7) and CHF patients with ischemic cardiomyopathy (311.6 +/- 120.4 pg/ml, n = 11; P < 0.001) vs. patients with nonfailing hearts and coronary artery disease (19.8 +/- 6.6 pg/ml, n = 11). hU-II-ir was significantly higher in the aortic root than in the pulmonary artery and femoral vein, with a nonsignificant trend for higher levels in the aortic root than in the femoral artery. The findings indicated that hU-II-ir is elevated in the aortic root of CHF patients and that hU-II-ir is cleared at least in part from the microcirculation.
authors.affiliation: Department of Medicine, University of Queensland, Prince Charles Hospital, Rode Road, Chermside, Queensland 4032, Australia. russell@medicine.uq.edu.au
authors.forename: Fraser D
authors.initials: FD
authors.lastname: Russell
authors.forename: Deborah
authors.initials: D
authors.lastname: Meyers
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Galbraith
authors.forename: Nick
authors.initials: N
authors.lastname: Bett
authors.forename: Istvan
authors.initials: I
authors.lastname: Toth
authors.forename: Philip
authors.initials: P
authors.lastname: Kearns
authors.forename: Peter
authors.initials: P
authors.lastname: Molenaar
mesh_terms: D016022:Case-Control Studies; D005260:Female; D045683:Furin; D006333:Heart Failure / Q000097:blood* / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction / Q000187:drug effects; D010446:Peptide Fragments / Q000097:blood; D011863:Radioimmunoassay; D013381:Subtilisins / Q000494:pharmacology; D014579:Urotensins / Q000097:blood* / Q000737:chemistry
chemical_list: D010446:Peptide Fragments; D014579:Urotensins; C029677:urotensin II; D013381:Subtilisins; D045683:Furin