ABSTRACT
Objective: To study the correlation between angiotensin II type1 receptor autoantibodies (AT1-AAs) and the onset risk in patients with essential hypertension (EH) combiningacute coronary syndrome (ACS). Methods: Our research included in 4 groups: EH+ACS group,n=28, ACS group, n=29, EH group,n=26 and Control group,n=23 normal subjects. Serum levels of AT1-AAs were examined by ELISA; high sensitivity C-reactive protein (hs-CRP), blood levels of lipids and glucose were also measured and compared among different groups. The correlations between AT1-AAs and blood lipids, glucose, hs-CRP were studied by multiple linear regression analysis. Results: Compared with Control group, ACS group had similar level of AT1-AAs (0.26±0.09) vs (0.21±0.06),P=0.105; while EH+ACS group and HE group had increased AT1-AAs level as (0.40±0.005) and (0.33±0.10),P=0.001 andP=0.02 respectively; AT1-AAs level was higher in EH+ACS group than HE group,P=0.044. In addition, serum AT1-AAs level was positively related to hs-CRP in EH+ACS group, ACS group and EH group (r=0.589,r=0.503 andr=0.273, allP<0.01). Conclusion: Serum AT1-AAs level was positively related to the onset risk in patients with EH combining ACS; AT1-AAs was also related to hs-CRP at certain degree.
ABSTRACT
Sestrin-2 (SESN2) is involved in the cellular response to different stress conditions. However, the function of SESN2 in the cardiovascular system remains unknown. In the present study, we tested whether SESN2 has a beneficial effect on vascular endothelial damage induced by angiotensin II (AngII). Firstly, we found that AngII induces expression of SESN2 in human umbilical vein endothelial cells (HUVECs) in a time-dependent and dose-dependent manner. We also found that knockdown of SESN2 using small RNA interference promotes cellular toxicity of AngII, as well as a reduction in cell viability, exacerbation of oxidative stress, and stimulation of apoptosis. In addition, our results show that the c-Jun NH (2)-terminal kinase (JNK)/c-Jun pathway is activated by AngII. Inhibiting the activity of the JNK pathway abolishes the increase in SESN2 induced by AngII. Importantly, overexpression of c-Jun promotes luciferase activity of the SESN2 promoter. These findings suggest that the inductive effect of SESN2 is mediated by the JNK/c-Jun pathway. Our results indicate that the induction of SESN2 acts as a compensatory response to AngII for survival, implying that stimulating expression of SESN2 might be an effective pharmacological target for the treatment of AngII-associated cardiovascular diseases.
Subject(s)
Angiotensin II/pharmacology , Human Umbilical Vein Endothelial Cells/pathology , JNK Mitogen-Activated Protein Kinases/metabolism , Nuclear Proteins/biosynthesis , Vasoconstrictor Agents/pharmacology , Aldehydes/metabolism , Apoptosis/drug effects , Apoptosis/genetics , Cell Survival/drug effects , Cells, Cultured , Humans , JNK Mitogen-Activated Protein Kinases/antagonists & inhibitors , JNK Mitogen-Activated Protein Kinases/biosynthesis , L-Lactate Dehydrogenase/metabolism , MAP Kinase Signaling System/drug effects , Nuclear Proteins/genetics , Oxidative Stress/drug effects , Oxidative Stress/genetics , Promoter Regions, Genetic/genetics , RNA Interference , RNA, Messenger/biosynthesis , RNA, Small Interfering , Reactive Oxygen Species/metabolism , Up-RegulationABSTRACT
Objective:To analyze the clinical therapeutic effect and safety of large dosage of valsartan on chronic heart failure (CHF).Methods:A total of 106 CHF patients hospitalized in our department were chosen and ran-domly divided into routine dose group (n=53,received routine dosage of valsartan,80mg,once/d)and large dose group (n=53,received large dosage of valsartan,80mg,twice/d)accerding to number table.Both groups received anti-heart failure treatment for six months according to the guidelines.After treatment,plasma N terminal pro brain natriuretic peptide (NT-proBNP)level was measured,left ventricular end-systolic diameter (LVESd),left ventricu-lar end-diastolic diameter (LVEDd),interventricular septal thickness (IVST)and left ventricular posterior wall thickness (LVPWT)were measured by color Doppler echocardiography,and all patients received 6min walking test. Therapeutic effect and incidence rates of adverse reactions were compared and analyzed between two groups after treatment.Results: Compared with routine dose group,there were significant reductions in NT-proBNP level [(3042.6±116.3)pmol/L vs.(2565.8±98.2)pmol/L],LVESd [(34.5±2.2)mm vs.(29.4± 2.0)mm], LVEDd [(55.1±2.9)mm vs.(50.2±2.5)mm],IVST [(12.9±1.8)mm vs.(10.7±1.2)mm]and LVPWT [(11.8±1.1)mm vs.(10.9±0.9)mm];significant rise in 6min walking distance [(271.2±24.9)m vs.(367.7 ±22.3)m]and total effective rate (43.40% vs.62.26%)in large dose group,P 0.05).Conclusion:Large dos-age of valsartan is more effective and is safe in treatment of chronic heart failure.
