Abstract:Aim To investigate the effects of ouabain or atrial natriuretic peptide （ANP） on angiotensinⅡ secreted by artery smooth muscle cells （ASMC） in WKY rats and spontaneously hypertensive rats （SHR）. Methods The thoracic ASMC isolated from SHR and WKY rats were cultured and interfered with different concentrations of ANP or ouabain （1×10－9 mol/L, 1×10－8 mol/L and 1×10－7 mol/L） respectively. The levels of angiotensinⅡ in culture-medium were measured by radioimmunoassay before and after 3, 6, 12, and 24 hours of using ouabain or ANP （1×10－7 mol/L）. Results AngiotensinⅡ level in WKY rats was lower than that in SHR. After using ouabain, angiotensinⅡ level of two kinds of rats was remarkably increased, but in WKY rats angiotensinⅡ level reached the peak after 12 hours, while in SHR reached the peak after 6 hours. With the increasing concentration of ouabain, angiotensinⅡ level in WKY rats was increased in a concentration-dependent manner, and in SHR increased in a concentration-independent manner. After using ANP, the level of angiotensinⅡ of two kinds of rats was significantly increased, but in WKY rats reached the peak after 3 hours, and in SHR increased in a time-dependent manner. With the increase of concentration of ANP, the level of angiotensinⅡ went down in WKY rats, whereas went up in SHR. Conclusions Ouabain or ANP can promote the secretion of angiotensinⅡ of ASMC in both WKY rats and SHR, and the secretion peak of angiotensinⅡ induced by ouabain is in advance in SHR. The secretion of AngiotensinⅡ induced by ANP is significantly abnormal in SHR.

Abstract:Aim To explore effects and mechanism of panax notoginseng saponin (PNS) on hypertrophic myocardium caused by abdominal aorta constriction(AAC) in rats. Methods Rat left ventricular hypertrophy was induced by abdominal aorta constriction in 75 rats, and 15 rats were randomly taken as sham group. One week after surgery, rats were divided into 4 groups: model group (abdominal aorta constriction rats), low-dose PNS group (50 mg/kg), middle-dose PNS group (100 mg/kg) and high-dose PNS group (150 mg/kg). After accepting therapy for 11 weeks, the hemodynamics of all animals was detected the left ventricle was recorded to calculate left ventricular hypertrophic parameters including left ventricular hypertrophy index (HMI, the ratio of the heart and body weight and LVMI, the ratio of the left ventricular weight and body weight) pathological section was stained by hematoxylin-eosin(HE) the lactic acid (LAC) and free fatty acids(FFA) were measured the mRNA expression of heart atrial natriuretic peptide (ANP) was observed through reverse transcription-polymerase chain reaction (RT-RCR) the contents of adenosine triphosphate (ATP), adenosine diphosphate(ADP) and adenosine monophosphate (AMP) in rat were detected by high performance liquid chromatography (HPLC). Results Compared with the AAC model group, PNS was able to inhibit cardiac hypertrophy, ameliorate hemodynamics, the expression of atrial natriuretic peptide was decreased, the lactic acid (LAC) and free fatty acid (FFA) levels was decreased, and the content of ATP, ADP and AMP was largely increased. Conclusions PNS protection against left ventricular hypertrophy elicited by abdominal aorta constriction in rats is mediated, at least in part, via ameliorate energy metabolism.

Abstract:Aim To investigate the association between the polymorphisms of angiotensinogen gene(AGT235),angiotensin converting enzyme gene(ACEI/D),atrial natriuretic peptide gene(ANP2238) and essential hypertension in a southern Chinese Han population.Methods Performed by gene chip technology,the genotypes of 81 essential hypertensive people and 120 control people were measured to analyze the polymorphisms of AGT235,ACEI/D and ANP2238.Results A significantly higher frequency of ACEI/D DD genotype was observed in hypertensive group(48.1% vs 4.2%,P<0.001) than in control group.In hypertensive group,the frequency of AGT235 TT genotype and ANP2238CC genotype was respectively 53.1% and 6.1%,while it was respectively 45.8% and 8.3% in control group.No significant differences were observed(P>0.05).Conclusion The polymorphism of ACEI/D gene is related to essential hypertension.

Abstract:Aim Cardiotrophin-1(CT-1) is a member of interleukin-6(IL-6) family of cytokines.CT-1 plays a role in inducing cardiomyocyte hypertrophy and promoting cardiomyocyte viability.We sought to elucidate effect of CT-1 inducing atrial natriuretic peptide (ANP) mRNA expression and its underlying mechanism in cultured neonatal rat cardiomyocyte. Methods The cardiomyocytes of neonatal rat were isolated and cultured with method of pre-plating for different time.The ANP gene of cardiomyocytes was measured with reverse transcription polymerase chain reaction(RT-PCR) approach. Results The ANP/GAPDH ratio of cardiac myocytes were increased by CT-1 in a dose-dependent manner(10-9,10-8 and 10-7 mol/L) in cultured neonatal rat cardiomyocytes.The ratio were respectively 1.18±0.14,1.58±0.20 and 2.03±0.30.And the ANP/GAPDH ratio were also augmented by CT-1 in a time-dependent manner(1,3,5 d,10-8 mol/L),respectively 1.16±0.18,1.47±0.17 and 1.97±0.24.Pretreatment of PD098059(50 μmol/L),a extracellular signal regulated kinase 1/2(ERK1/2) blocker,increased significantly ANP mRNA expression of cardiac myocytes induced by CT-1(ANP/GAPDH ratio 1.94±0.15),whereas Calphostin C,a protein kinase C(PKC) blocker,10 μmol/L,effected no significantly on this role induced by CT-1. Conclusion These results indicate that ANP mRNA expression induced by CT-1 increased significantly in a dose-dependent and a time-dependent manner in cultured neonatal rat cardiomyocytes.The MAPK(ERK1/2) signal pathway mediate the effect of CT-1.The PKC signaling molecule may no take part in directly the effect of CT-1.

Abstract:Aim To investigate the effects of soluble epoxide hydrolase inhibitor (sEHi) on cardiac hypertrophy. Methods The pathology changes of the hearts were observed in the pressure overload mice and pressure overload mice fed with sEHi. Semi-quantitative RT-PCR was used to measure the expression of hypertrophy genes: atrial natriuretic peptide (ANP), α-myosin heavy chain (α-MHC), β-myosin heavy chain (β-MHC), skeletal muscle alpha-actin (SM ɑ-actin). Western blot was used to measure the changes of nuclear factor (NF)-κB complex. Results sEHi could significantly decrease both heart weight/body weight ratio and dimension of left ventricular end systolic chamber, increase fractional shortening. It could also reduce hypertrophy gene expression, and inhibit the activity of NF-κB. Conclusion sEHi might inhibit pressure overload induced cardiac hypertrophy through the effects on NF-κB pathway.

Abstract:Aim To investigate the effects of atorvastatin on AngⅡ-induced hypertrophy myocytes and the changes of mRNA expression of peroxisome proliferators-activated receptorβ/δ in vitro. Methods Hypertrophy in neonatal rat cardiac myocytes(MC) was established with angiotensin Ⅱ(Ang Ⅱ) and treated with atorvastatin.The surface area of MC was analyzed by the aid of NIH Image J software,and the synthetic rate of protein in MC was detected by 3H-leucine incorporation.mRNA expression of atrial natriuretic peptide(ANP),brain natriuretic peptide(BNP) and peroxisome proliferatoractivated receptor beta/delta subtypes(PPARβ/δ) was measured by reverse transcription-polymerase chain reaction(RT-PCR). Results In the condition of hypertrophy,increases of surface area(p<0.01),mRNA expression of ANP,BNP(both p<0.01),and ~3H-leucine incorporation(p<0.01);and a decrease of mRNA expression of PPARβ/δ(p<0.01) in MC were detected,but no changes in treated with DMSO(p>0.05).Atorvatatin inhibited the changes above,reduced mRNA expression of ANP and BNP,elevated mRNA expression of PPARβ/δ in a dose-dependent manner(p<0.05). Conclusions It was suggested that atorvastatin has a potential role in the prevention and treatment of cardiac hypertrophy,and PPAR β/δ may be involved in it.