Research Between Congestive Heart Failure And Urotensin Ⅱ About Expression In Myocardial Cells And Levels Of Plasma

BackgroundCongestive heart failure(CHF) is the most severe status or the end-stage of all kinds of cardiovascular diseases and it is also one of cardiovascular diseases which is not easily cured. Although all kinds of treatments have improved hemodynamics abnormal and clinical feature, with aged its incidence and mortality are increasing. CHF is a clinical syndrome resulted from many factors, so it makes treatment difficult. It has proved that activated sympathetic nerve neurosecretory hormone and cytokines all participate in compensatory regulation. The balance changes of neurosecretory hormone including vasoconstictors and vasodilators activation is an important factor which determines prognosis of patients with CHF. So the changes of these vasoactive substances may be an important role in progress of CHF and evaluating its prognosis. Urotensin-II (U-II), a peptide isolated from the urophysis of teleost fish 35 years ago, is the endogenous ligand of the mammalian orphan receptor GPRl4/SENR. Recently, human homologues of both the receptor (UT-II) and the peptide (hU-II) have been discovered,it is the most potent mammalian vasoconstictor yet identified, in the order of ten-fold often more potent than that of endothelin-1. The biologic characteristic and distribution of urotensin II and its receptor(UT-II) provide basis of cardiovascular modulation, which showed that urotensin II may be a role in prognosis of cardiovascular diseases. But foreign studies on plasma levels and cardiovascular gene expression of urotensin II in patients with congestive heart failure are not consistent. The paper investigated the changes of plasma levels and relation of urotensin II and other vasoactive substances in patients with CHF. It proves that these vasoactive substances vary in the process of CHF. Although their changes are not the same, they allparticipate in compensatory regulation of CHF, so it may provide theory basis and objective guideline for diagnosis and treatment of CHF.Objective:1. We study changes of plasma levels of urotensin II in patients with CHF and our aim is to illustrate clinical signification and action of urotensin II.2. By studying relationship between urotensin II, proadrenomedullin N-terminal 20 peptide and atrial natriuretic peptide, it shows that these vasoactive substances act and antagonize one another in the process of CHF progression. We recognize that their changes exert on patho- physiological modulating mechanism of heart failure.3. We want to illuminate autocrine and/or paracrine action during heart failure regulation by studying expression of urotensin II in myocardial cells.Methods:1. Fifty-two patients (32 men and 20 women, 60.9?0.8 years old )with CHF and twenty age and gender-matched normal healthy subjects (10 men and 10 women, 61.9+14.8 years old )were studied. Heart function of all study subjects were mensurated by ultrasound cardiography, ejection fraction and the E/A ratio of left ventricle were mensurated.2. In brief, Blood samples for UII. PAMP and ANP assay were collected in chilled tubes containing EDTA and Aprotinin and immediately placed on ice. After centrifugation at 3000 rpm at 4癈 for 15 minutes, the plasma was decanted and stored at -70 癈 until analysis.3. Plasma UII PAMP and ANP levels of 52 patients with CHF and 20 control subjects were measured by radioimmunoassay.4. The models of acute myocardial infarction-induced heart failure were made with rabbits. We investigated changes of the haemodynamic parameters and expression of urotensin II protensin in the cardiomyocytes.Results:1. There were no significant differences in sex and age between CHF and controls. LVEF was significantly decreased in patients with CHF comparing with that in control subjects(48.04 + 11.44v5 64.81 +4.39,P<0.05); The worse the heart function is, the lower the rate of E/A and LVEF are.2. Plasma U II concentration was 4.28+1.21pg/mL in age-matched controls(n=20). Plasma UII concentration decreased to 1.48+1.0...