Objective To study the effect of angiotensin converting enzyme inhibitory peptides (ACEIP) on blood pressure of spontaneously hypertensive rats.Methods One hundred and four spontaneously hypertensive rats(SHR) were randomized to thirteen groups (n= 8,each group) and received one of following approaches:saline,captopril (10 mg/kg),low-dose (200 ?g/kg),medium-dose(400 ?g/kg) and high-dose (800 ?g/kg) of the three ACEIPs:VLPVP,KVLPVP,VLPVPR respectively.Thirty-two WKY rats were randomized to 4 groups(n=8 in each group),VLPVP,KVLPVP,VLPVPR (800 ?g/kg by gavage) and saline were administrated.The systolic blood pressure was measured before and after the administration of ACEIP.Results Compared with the control group,medium-dose and high-dose of VLPVP,KVLPVP and VLPVPR reduce blood pressure in hypertensive rats and the effect can last for above 6 hours [decline of blood pressure:high-dose:(40.9?15.7),(38.0?21.3) and (43.2?12.6) mmHg;medium-dose:(28.3?23.0),(24.7?21.5) and (26.2?9.9);control:(8.5?5.1),(6.2?4.1) and (7.1?5.5)mmHg;all P0.05].Conclusion Recombinant ACEIP acutely reduce high blood pressure in SHR,the antihypertensive effects persist for at least 6 hours,with no effect on normotensive WKY rats.

Objective To investigate the molecular mechanisms for the development of cardiac hypertrophy in hypertension by scanning the expression profile of microRNA (miRNA) in the left ventricular hypertrophic tissue in spontaneously hypertensive rats(SHR)using miRNA microarray chip technique.Methods 17-week-old male SHR with left ventricle hypertrophy (LVH) (n=10) and 8-week-old male SHR without LVH were employed in this study (n=10).Left ventricular mass index (LVMI),HE staining and measurement of transverse diameter of myocardium (TDM) were used to evaluate LVH.The mRNAs of the two groups were extracted from left ventricle tissue and the differential expression of miRNA was detected by using miRNA microarray chip.Results LVMI and TDM were greater in rats with LVH vs without [LVMI(2.87?0.15)vs(2.17?0.14)mg/g;TDM(15.32?0.61)vs(12.01?0.43)?m,P

Background Hypertension is a multigenetic inheritable disease.Gene therapy by regulating gene expression showed long term effects and less side effects,and has been emerged to be a potential and prospective treatment.Objective To investigate the effects of retroviraladeno-associated virus vector containing shRNA targeted on the AT1R gene (rAAV-AT1R-shRNA) on blood preesure(BP) in renal hypertensive rats,and the inhibitory effect of RNA interference (RNAi) on AT1R mRNA expression in renal hypertensive rats.Methods Two-kideny one-clip (2K1C) renal hypertension (RH) were established in SD rats and randomly to receive rAAV-AT1R-shRNA,1.5?109 particles/mL(n=12,ip),as treated group or retroviral vector (rAAV-EGFP),2.9?109 particles/mL,ip,as vehicle group,normal SD rats served as controls (n=12).SBP was measured before and after treatment.Animals were euthanized and blood,brain,heart,liver,kidney,aorta and adrenal gland were collected to identify the sites of rAAV-AT1R-shRNA expression by fluorescence microscope.Angiotensin Ⅱwas assessed by radioimmunology.Results 24 hours after single injection of rAAV-AT1R-shRNA,SBP was reduced by (22.3?5.5)mmHg compared to before intervention (P

2016.0 ng/L group (n=85) and followed up for average 371 days (90-540 d).Cardiac death or decompensated heart failure(HF) readmission were counted as advease events end-point for the purpose of this analysis.Results At follow up,76 patients had the cardiac events (26 patients died from cardiovascular causes and 50 patients being rehospitalization).No differences in admission NT-proBNP between patients with and without cardiovascular events.However,patients with high pre-discharge NT-proBNP(3872.0 vs 1306.0 ng/L,P

Backgroup and objective Angiotensin-converting enzyme 2 (ACE2) is the first known homologue of human ACE gene up till now,however,its regulatory role in oxidative stress remains unclear.Our aim is to in- vestigate the effects of recombinant ACE2 gene transfer on the expression of p22~(phox),a key subunit of NADPH oxi- dase,and malonyldialdehyde (MDA) levels induced by angiotension(Ang) Ⅱ in cultured human endothelial cells. Methods A recombinant plasmid encompassing human ACE2 gene (pACE2) was constructed and transfected into these cells.The mRNA and protein levels of p22~(phox) in endothelial cells were determined by real-time PCR and Western blotting,respectively.MDA contents were measured by thiobarbiturie acid colorimetrie method in cells. Results The mRNA and protein expressions of p22~(phox) were drastically enhanced after exposures of endothelial cells to Ang Ⅱ(100 nmol/L) and Ang Ⅳ(100 nmol/L),accompanied by an increase in MDA contents (n=6,P

75%(more than 2-vessel disease) and 50 persons with angia and non-diabetes were selected as control.Results The level of NT-proBNP was significantly higher in stable angina patients with diabetes(750?80 ng/L) than that in stable angina patients without diabetes(450?75 ng/L)(P

Background Familial hyperaldosteronism type Ⅱ(FH-Ⅱ) is characterized by autosomal dominant inheritance and hyperaldosteronism.Linkage analysis demonstrated chromosome 7q22 most likely harbor the genetic defect.Objective To identify the disease locus in a Chinese pedigree with FH-Ⅱ using genetic linkage analysis.Methods Haplotypes of the FH-Ⅱ pedigree were analyzed using four microsatellite markers(D7S531,D7S2521,D7S511,D7S481) at 7p22 to determine the critical region,and multipoint logarithm of odds(LOD) scores were calculated to assess linkage with FH-Ⅱ.Results Several members(affected members) in the family had hypertension,hypokalemia,hyperaldosteronism,low renin activity.Hypertension and hypokalemia was improved by spironolactone test.Dexamethasone suppression test was performed but without clinical or hyperaldosteronism improvement in three affected members,confirmed FH-Ⅱ family pedigree.The same haplotypes D7S531(ac,n=24)-D7S2521(ac,n=11)-D7S511(ca,n=21)-D7S481(ac,n=16) were shared by all known affected members and one suspicious member,but also by one unaffected member of the family,making it unlikely that this region contains the causative gene mutation.In this FH-Ⅱ family,the LOD scores of the four markers were

Objective The effect of combined treatment of statins and calcium channel blockers(CCB) in elderly patients with isolated systolic hypertension(ISH) are not well understood.The purpose of the present study was to assess the additive effect of benidipine-atorvastatin combination therapy in old patients with ISH.Methods Ninety patients with ISH were randomized to receive: placebo(n=15),benidipine treatment(4-8 mg/d,n=25),atorvastatin(20 mg/d,n=25) and benidipine plus atorvastatin treatment(4-8 mg/d+20 mg/d,n=25) for 5 months.Serum concentrations of IL-6,IL-8,hsCRP,flow-mediated dilatation of the brachial artery,urine microalbumin,left ventricular mass index(LVMI),carotid intima-media thickness(CIMT),BP and plasma lipids profiles were examined before and after treatment.Results After 5-months of treatment,the combination treatment significantly reduced IL-6(IL-6 reduction magnitude,combination group: 6.5+6.3 ng/L vs benidipine group: 3.1?3.2 ng/L vs atorvastatin group: 3.3?2.3 ng/L,P

Background Left atrium size was reported as a marker for ventricular diastolic dysfunction and predictive risk factors for cardiovascular disease.Objective To analyze the relations between left atrial(LA) size and left ventricular(LV) diastolic function echocardiographically in rabbit model with LV dysfunction while with normal LVEF.Methods LV pressure overloaded animal model was established by abdominal aorta constriction in 18 New-Zealand rabbits(model group) which developed LVH with normal EF with 8 healthy rabbits as normal controls.LA dimension and volume(LAD,LAV),left ventricular dimension(LVD) and wall thickness(IVST,PWT),Transmitral inflow E and A,and mitral annulus velocities Ea and Aa were determined by echocardiography.LVEDP was measured within 24 hours after echo examination by catheterization.Results ①Increased LVD,IVST,PWT and LA size were found in model group(P

LAD(OR=1.209). Conclusion Left atrial diameter was independent risk factor for ischemic stroke in hypertensive patients.