The dynamic changes of angiotensin Ⅱ and atrial natriuretic factor levels in hypothalamus and infarct volume of rats with foc

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Role of angiotensin Ⅱ and angiotensin Ⅱ receptors in vascular smooth muscle cell migration in vitro

ObjectiveTo determine the biotic effects of angiotensin Ⅱ (Ang Ⅱ) on the migration of rat smooth muscle cells (VSMCs) and investigate the mechanisms involved in the development of vascular injury. Methods VSMCs isolated from aortic media of Wistar rats and cultured by the modified explant method were adopted. In the presence and absence of Ang Ⅱ, the expression of Ang Ⅱ receptor (ATR) and reorganization of the actin cytoskeleton and focal adhesion of VSMCs were studied by an immunocytochemistry technique and fluorocytochemistry technique. Migration assays were performed with a modified Boyden’s chamber. The effects of AT(1)R antagonist (CV- 11974), AT2R antagonist (PD123319) on the aforementioned target were studied. Results VSMCs migration was stimulated by adding Ang Ⅱ. The dynamic reorganization of actin cytoskeleton and focal adhesions may be an important mechanism by which Ang Ⅱ facilitates VSMCs motility. The expression of AT(1)R in VSMCs could be upregulated initially after treatment with Ang Ⅱ, then decreased gradually. The expression of AT(1)R was downregulated by AT(1)R antagonists. The effect of Ang Ⅱ on VSMCs migration was mediated by AT(1)R, while AT2R had no significant effect. Conclusions The dynamic reorganization of focal adhesions and the actin cytoskeleton is required for Ang Ⅱ- induced VSMCs migration. This effect is mediated by AT(1)R.     

Relationship between remodeling and function of left ventricle and angiotensin Ⅱ AT1 receptor expression after myocardial infarction in rats

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Effects of Serum Containing Xinlikang (心力康) on Angiotensin Ⅱ Induced Hypertrophy in Cultured Neonatal Rat Cardiomyocytes

Objective: To evaluate the effects of Xinlikang (心力康,XLK) on angiotensinⅡ(AngⅡ) induced hypertrophic cultured neonatal rat's cardiomyocyte (CMC). Methods: Primary cultured neonatal rat's CMCs with the purity certified by immunohistochemical technique, were divided into three groups. Rats in the normal control group were untreated; those in the model group were established into hypertrophic models but underwent no treatment; and those in the XLK group were established to hypertrophic models and treated with XLK containing serum obtained from rats with aorta coarctation after 8 days of feeding with XLK. MTT and phase-contrast microscope were used to evaluate the effect of XLK on cell activity, pulsating rhythm and surface area; Atrial natriuretic peptide (ANP) expression was determined by radioimmunoassay; Protein content was determined by Bradford method; and DNA synthesis was detected by flow cytometric assay. Results: Immunohistochemistry results showed that more than 90% of the cells wereα-sarcometin actin stained positive cells. No significant effect of XLK on normal CMC was found. AngⅡcould significantly induce hypertrophy in CMCs, and XLK could significantly decrease the increased surface area and the accelerated pulsating rate in them. ANP expression was 780±38 Mg/L in the model group, and 430±23μg/L in the control group, and the elevated expression of ANP in model rats was significantly decreased in the XLK group;The DNA content in the G0/G1 and G2/M phases was significantly enhanced and at the same time it was accompanied with increase of total protein content in the model rats after being stimulated by AngⅡfor 24 h, showing that serum-containing XLK could also significantly suppress total protein synthesis (P<0. 05). Conclusion: XLK could improve AngⅡmediated pathological growth of CMCs without influencing the growth of normal CMCs, suggesting that XLK is probably an effective drug for treatment of myocardial hypertrophy and heart failure.     

Blockades of angiotensin and aldosterone reduce osteopontin expression and interstitial fibrosis infiltration in rats with myocardial infarction

Background It has been reported that osteopontin has an important role in cardiac fibrosis and remodeling. However, its direct mechanisms remain unclear. The purpose of this study was to investigate the role of angiotensin and aldosterone blockades in cardiac osteopontin expression associated with cardiac remodeling in myocardial infarcted （MI） rats.
Methods Fifty SD rats that survived 24 hours after ligating left anterior descending coronary artery were randomly divided into three groups： MI-saline group （n=15, 5 ml/d）, MI-perindopril group （n=18, perindopril 2 mg·kg^-1·d^-1） and MI-spironolacton （n=-17, spironolacton 20 mg·kg^-1·d^-1）. A sham operation group （n=15） was selected as non-infarcted control. At 6 weeks after treatment, hemodynamic pararmeters and left ventricular function were measured with catheterization, interstitial fibrosis infiltration and cardiomyocyte diameters were evaluated histologically. Myocardium osteopontin protein expression level in the non-infarcted myocardium was detected by Western blotting.
Results No osteopontin protein was detected in the myocardium of sham-operation rats. High levels of osteopontin protein expression were detected in the MI-saline rats, but the levels were suppressed in the MI-perindopril and MI-spironolacton rats at 6 weeks following MI （P 〈0.01, respectively）. Compared with the sham operation group, all rats in the MI group showed marked interstitial fibrosis infiltration in the non-infarction area, higher ventricular weight/body weight ratio, significantly increased cardiomyocyte diameter （P 〈0.01, respectively）, and developed significant systolic and diastolic dysfunction as indicated by decreased left ventricular systolic pressure （LVSP） and ±dp/dt, as well as increased left ventricular end-diastolic pressure （LVEDP） （P 〈0.01, respectively）. Angiotensin and aldosterone blockades partly prevented cardiac fibrosis and systolic and diastolic dysfunction （P 〈0.01, respectively）. Conclusion Treatm     

Effects of Qindan Capsule (芩丹胶囊) on blood pressure, endothelin, calcitonin gene-related peptide and angiotensin-II in spontaneous hypertensive rats

Objective： To observe the hypotensive effects of Qindan Capsule （芩丹胶囊, QC） on spontaneous hypertensive rats （SHR） and its effect on the contents of endothelin （ET）, calcitonin gene-related peptide （CGRP） and angiotensin-Ⅱ （Ang-Ⅱ ） in plasma and vascular tissues, and to investigate the possible mechanism of QC in lowering blood pressure. Methods： Forty SHRs were divided into 5 groups： the high dosage QC group [QCHD, 750 mg/（kg.d） ], the low dosage QC group [QCLD, 150 mg/（kgd） ], the Niuhuang Jiangya Pill group [牛黄降压丸,, NJP, 200 mg/（kg.d）], the Captopril group [ 15 mg/（kgd）]and the model group, 8 in each group. Meanwhile, a normal control group consisting of 8 Wistar-Kyoto （WKY） rats was set up also. All the rats were administered with medicine level of ET, CGRP and Ang-Ⅱ in plasma and Ang-Ⅱ rats after 12 weeks of treatment. Results： The leve through gastrogavage. Systolic blood pressure （SBP）, in tissues of mesenteric artery were detected in all the of SBP after treatment in the QCHD group was lower than that in the model group （ P〈0.01 ）, but with no significant difference as compared with that in the Captopril group and the NJP group （P〉0.05）. After treatment, the plasma level of ET was lower and CGRP higher than those in the model group （both P〈0.05）, and also higher than those in the NJP and Captopril group （both P〈0.05）. As for the content of Ang- Ⅱ , in mesenteric arterial tissues, it was lower in the QCHD group than that in the model group （ P〈0.05）, but in plasma, it showed no significant difference between the two groups （P〉0.05）. Conclusion： QC has a satisfactory hypotensive action on SHR rats, and its mechanism may be associated with the regulation on plasma vasoactive peptide and regional renin-angiotensin system.     

Effect of pharmaceutical intervention on AT1R, AT2R, ERK and JNK activity in chronic hibernating myocardium in rabbits

Objective： To investigate in chronic hibernating myocardium in rabbits and the influence and significance of captopril, betaloc, valsartan in angiotensin Ⅱ subtype 1 receptor（AT1R）, angiotensin Ⅱ subtype 2 receptor（AT2R）, extracellular signal regulated kinase 1/2 （ERK1/2）, c-Jun N-terminal kinase（JNK）. Methods： The model of chronic hibernating myocardium（CHM） was established. The changes of AT1R, AT2R, ERK1/2, JNK in different groups were assessed by western blotting and immunohistochemistry. Results： The amount of AT1R decreased while AT2R increased in the CON group compared with in sham group, and both AT1R and AT2R decreased in drug groups compared with the CON group. The content of ERK had no change in each group, while that of ＂expression＂ p-ERK increased in CON group compared with in sham group, and was lower in drug intervention groups than in CON and sham groups. The contents of JNK and p-JNK decreased in CON and drug intervention groups compared with in sham group. The protein levels of JNK, p-JNK in drug intervention groups were lower than in the CON group. Three drugs can inhibit interstitial fibrosis and reduce apoptotic cells. The expression levels in the groups（with different doses） had statistical difference as well as between groups of captopril and other drugs; however the results between betaloc and valsartan had no significant difference. Conclusion： AT1R, AT2R may be the upper stream receptor of ERK and JNK and may participate in generation and evolution of CHM. Captopril, valsartan and betaloc may preserve CHM by inhibiting ATIR, AT2R and JNK activity.     

Association of coagulation factor Ⅶ with the risk of myocardial infarction in the Chinese

Objective To elucidate the association of plasma factor Ⅶ coagulant activity (FⅦc) w it h the risk of myocardial infarction (MI) and to assess the influence of factor Ⅶ gene MspI polymorphism and lipid metabolism on FⅦc in the Chinese.Methods A total of 137 patients with angiographically confirmed MI and 125 healthy indiv iduals were evaluated retrospectively. Plasma FⅦc was measured by one-sta ge prothrombin time, and FⅦ genotype was determined after MspI digestion of polym erase chain reaction-amplified genomic DNA. Serum lipid levels were assessed b y routine methods.Results MI patients had significantly higher levels of FⅦc (119.5%±22.7% vs 99. 9% ±21.8%, P&lt;0.01) and total serum cholesterol (5.80±1.06 mmol/L vs 5.5 3±1.08 mmol/L, P&lt;0.05) than controls, but only FⅦc independently co rrelated with the risk of MI (OR=1.04, P&lt;0.01). There were no significant di fferences in FⅦ genotype or allele frequency between patients and controls ( P&gt;0.05). Subjects with the Gln353 allele were associated with significantly lower FⅦc levels than Arg353 homozygotes (99.7%±19.3% vs 111.4%±24.6% , P&lt;0.05). Serum triglyceride was positively correlated with plasma FⅦc in both control (r=0.25, P&lt;0.01) and case (r=0.87, P&lt;0.01) gro ups, but this correlation was restricted to Arg/Arg genotype (r=0.68, P &lt;0.01). A significant correlation of total serum cholesterol with FⅦc onl y appeared in Arg/Arg homozygotes (r=0.17, P&lt;0.01).Conclusions Our findings support the role of plasma FⅦc as a risk factor for MI in Chin es e. Plasma triglyceride and FⅦ gene MspI polymorphism are two independent d eter minants of FⅦc. Assay of this polymorphism will be helpful in determining who will benefit most from lipid-lowing therapy.     

Growth Inhibition and Apoptosis Induction in Human Hepatoma Cells by Tanshinone Ⅱ_A

Summary:In order to study the effect of tanshinone Ⅱ_A on growth and apoptosis in human hepatomacell line BEL-7402 in vitro,the human hepatoma cell line BEL-7402 was treated with tanshinone Ⅱ_Aat various concentrations for 72 h.Growth suppression was evaluated by MTT assay;apoptosis-relat-ed alterations in morphology and biochemistry were ascertained under cytochemical staining(Hoechst33258),transmission electron microscopy(TEM),and DNA agarose gel electrophoresis.Apoptoticrate was quantified by flow cytometry(FCM).The results showed thst Tanshinone Ⅱ_A could inhibitthe growth of hepatoma cells in a dose-dependent manner,with IC_(50) value being 6.28μg/ml.Aftertreatment with 1—10 μg/ml tanshinone Ⅱ_A for 72 h,BEL-7402 cells apoptosis with nuclear chro-matin condensation and fragmentation as well as cell shrinkage and the formation of apoptotic bodieswere observed.DNA ladder could be demonstrated on DNA electrophoresis.FCM analysis showedhypodiploid peaks on histogram,and the apoptotic rates at 5     

三类降压药物对高血压大鼠心肌细胞凋亡及左室重构的对比研究

目的 :评价氯沙坦、福辛普利、氨氯地平对自发性高血压大鼠 (SHR)心肌细胞凋亡及左室重构的效应。方法 :将 40只 16周龄SHR随机分为氯沙坦治疗组 (SHR -L)、福辛普利治疗组 (SHR -F)、氨氯地平治疗组 (SHR -A)及空白对照组 (SHR -C)。采用末端脱氧核糖核苷酸转移酶介导dUTP缺口末端标记、放免及病理检查方法对SHR治疗 8周、16周心肌细胞凋亡指数 (APOI)、血浆和组织血管紧张素II(PAngII,MAngII)及左室重构指标检测。结果 :①各治疗组治疗 8周、16周收缩压均明显下降 ,组间差异无显著性 ;各治疗组左室重量 (LVW)、左室重量指数 (LVMI)均有显著性改善 ,SHR -F组治疗 16周较其他两组LVMI显著减低。②仅SHR -F组治疗 8周APOI显著性下降 ,治疗 16周各治疗组APOI均有显著下降 ,尤以SHR -F组下降明显。③SHR -L组治疗 8周及 16周PAngII,MAngII显著增加。SHR -F组治疗 8周MAngII显著下降 ,治疗 16周SHR -F ,SHR -A两组MAngII均明显下降 ,且前组较后组下降显著 ,但对PAngII无明显影响。结论 :3药物均能有效逆转心脏肥厚及抗心肌细胞凋亡 ,其中以福辛普利显著。上述作用可能是拮抗心肌组织肾素 -血管紧张素 -醛固酮系统的效应。     

洛沙坦抑制急性心肌梗死大鼠心肌纤维化的作用机制

目的 观察洛沙坦对急性心肌梗死大鼠心肌组织中盐皮质激素受体(MR)mRNA及心肌纤维化的影响.方法 结扎左冠状动脉致急性心肌梗死大鼠模型.随机分为急性心梗组和洛沙坦治疗组,而对照组为仅打开心包腔而未行冠状动脉结扎大鼠.在洛沙坦治疗4周时,用超声心动图和血流动力学指标评价心脏功能,心肌Masson染色法测定心肌胶原密度,放射性免疫法测定心肌组织中血管紧张素Ⅱ(AngⅡ)、醛同酮(Ald)含量,实时荧光定量PCR检测心肌MRmRNA表达.结果 (1)急性心梗组大鼠心肌组织中AngⅡ、Ald含量较对照组显著增加,心肌MRmRNA表达显著升高,同时心肌胶原密度显著增加(P<0.01).(2)洛沙坦治疗4周后,治疗组大鼠心肌组织中AngⅡ、Ald较急性心梗组显著减低(P<0.05),MRmRNA表达显著降低,心肌胶原密度也有显著降低(P<0.01).结论 洛沙坦可以抑制急性心肌梗死大鼠心肌组织中Ald信号通路.并且还可能通过下调心肌MRmRNA表达来抑制心肌纤维化.     

慢性低氧致大鼠右心室心肌纤维化作用及其机制的研究

目的 探讨慢性低氧大鼠右心室心肌纤维化的表现特征及其发生机制。方法 将40只Wistar大鼠分为两组。每组20只。慢性低氧组：大鼠置于模拟5000m的高原地区饲养30和60d，每天低氧8h；对照组：在平原地区饲养30和60d。测定左、右心室收缩压、动脉血氧分压、红细胞压积、心室重量指数、心肌胶原浓度和含量及心肌Ⅰ／Ⅲ型胶原比值，观察心肌形态学变化。结果 慢性低氧组PaO2下降，右心室收缩压及右心室重量指数增高，右心室心肌胶原浓度和含量及心肌Ⅰ／Ⅲ型胶原比值明显增高，而左心室则无明显变化。病理学检查示慢性低氧组右心室出现心肌内血管周围纤维化和局灶性纤维化。结论慢性低氧可导致右心室心肌纤维化。右心室压力负荷增加是其发生的重要因素。     

血管紧张素(1-7)对不同模型高血压大鼠左心室结构的影响

目的 探讨血管紧张素(1-7)[Ang(1-7)]对单纯压力负荷增加及肾素.血管紧张素.醛同酮系统(RAAS)激活的高血压模型左心室肥厚及心肌纤维化的影响及其机制.方法 建立二肾一夹(2K1C)及肾下主动脉缩窄(INAC)模型,应用微渗泵植入技术,使Ang(1-7)进行不同时间(14、28 d)的体内干预,采用定性及定量分析的方法 检测Ang(1-7)对这2种高血压模型早期(14 d)和晚期(42 d)左心室心肌细胞及纤维化程度的影响.结果 对2K1C和INAC动物模型,早期其左心室质量(LVW)、左心室质量指数(LVI)及左心室心肌细胞横断面积(LCA)均较对照组明显增加(P<0.05),晚期上述指标增加更为显著(P<0.01);Ang(1-7)可使2K1C动物模型的上述指标均显著下降(P<0.05),但对INAC动物模型,Ang(1-7)使其上述指标在早期显著下降(P<0.05),晚期略有下降(P>0.05).对2K1C动物模型,早期已出现明显的心肌纤维化(P<0.05),晚期更为显著(P<0.01);Ang(1-7)可明显抑制早期的间质及血管周围纤维化(P<0.05),在晚期,Ang(1-7)可明显抑制血管周围纤维化(P<0.05),但对间质纤维化,虽有下降趋势,但不明显(P>0.05).对IN-AC动物模型,早期心肌纤维化并不显著(P>0.05),晚期则有明显表现(P<0.05),Ang(1-7)可有效抑制问质和血管周围纤维化(P<0.05).结论 Ang(1-7)可预防改善这2种高血压模型的左心室肥厚和心肌纤维化,但对2种模型不同时期的改善程度不同,提示Ang(1-7)可能具有不同的作用机制.     

氯沙坦、福辛普利对高血压大鼠心肌纤维化、血管紧张素Ⅱ及左室重构的影响

目的：评价氯沙坦、福辛普利对自发性高血压大鼠（SHR）心肌纤维化=、左室重构及血浆和心肌组织中血管紧张素Ⅱ的效应。方法：16周龄SHR随机分为3组,即氯沙坦治疗组（SHR-L组）、福辛普利治疗组（SHR-F组）、空白对照组（SHR-C组）,每组各10只。分别采用病理检查及放射免疫测定方法对治疗8周、16周的SHR心肌胶原容积分数（CVF）和心肌血管周围胶原面积（PVCA）、血浆和组织中血管紧张素Ⅱ进行检测。结果：在治疗8周、16周后,两治疗组的收缩压较对照组均有明显下降;治疗组组间比较差异无显著性（P＞0.05);心脏重量（HW）、心脏重量指数（HWI）、左室重量（LVW）、左室重量指数（LVMI）均有显著性改善,且治疗16周后SHR-F组较SHR-L组LVMI显著性降低（P＜0.05)。两治疗组CVF和PVCA与对照组比较明显下降（P＜0.01)。治疗16周后SHR-F组CVF较SHR-L组下降更明显。SHR-L组血浆及心肌组织中AngⅡ显著增加,而SHR-F组心肌组织AngⅡ显著下降,但对血浆AngⅡ无明显影响。结论：氯沙坦、福辛普利均能有效逆转心脏肥厚及抗心肌纤维化,以福辛普利作用显著。其作用机制可能与拮抗心肌组织中肾素-血管紧张素-醛固酮系统（RAS）效应有关。     

缬沙坦对自发性高血压大鼠心肌细胞凋亡的影响

目的　研究遗传性高血压及左室肥厚过程中心肌细胞凋亡及特异性AT1受体拮抗剂缬沙坦对心肌细胞凋亡的影响 ,探讨高血压左室肥厚及心肌细胞凋亡的可能机制。方法　选用 10周龄自发性高血压大鼠 (SHR) 30只 ,随机均分为缬沙坦治疗组 (SHR +缬沙坦组 )和非治疗组 (SHR无药组 ) ,以Wistar鼠作为正常血压对照组。SHR+缬沙坦组给予特异性血管紧张素Ⅱ 1型受体拮抗剂缬沙坦 2 0mg/ (kg·d) ,溶解于特制饮水器中每天 1次胃管灌入。其他两组每天饮用水 10ml/kg灌胃。观察期限为 12周 ,每 2周测鼠尾动脉血压。 12周后采用TUNEL法检测大鼠心肌细胞凋亡情况。结果　SHR随周龄增长 ,血压增高、心肌肥厚的同时发生心肌细胞凋亡 ,缬沙坦用药 12周后 ,SHR心肌细胞凋亡显著降低至接近Wistar组 (P <0 .0 5 )。结论　心肌细胞凋亡是代偿性心肌肥厚发展为心力衰竭的可能机制之一。高血压病早期缬沙坦在降压同时有效抑制心肌细胞凋亡     

氯沙坦对大鼠急性心肌梗死的保护作用及其机制

探讨血管紧张素Ⅱ受体1（AT1R）阻断剂氯沙坦对急性心肌梗死（AMI）大鼠心肌损伤和心肌修复的影响,并阐明其作用机制。     

Effect of angiotensin Ⅱ type Ⅰ receptor blocker losartan on bone deterioration in orchiectomized male hypertensive and normotensive rats

Background Epidemiological study showed that the use of angiotensin-converting enzyme inhibitors was associated with higher bone mineral density (BMD) in older people,especially male subjects,which sug...     

洛沙坦在大鼠门脉高压性胃病中的作用

目的:探讨洛沙坦在大鼠门脉高压性胃病中的作用及相关机制.方法:48只SD大鼠随机均分为假手术组、门静脉高压胃病模型组、洛沙坦治疗组、洛沙坦预防组.采用门静脉主干部分结扎 左肾上腺静脉结扎法复制门静脉高压胃病模型.测量门静脉压力(PVP)、胃损伤指数(GI)、胃病理评分(PI),用原位杂交技术检测各组大鼠胃部血管紧张素Ⅱ1型受体(AT1R)表达分布和变化情况.结果:治疗组和预防组的PVP,GI和PI较模型组明显下降(P＜0.01),血浆Ang Ⅱ较模型组明显升高(P＜0.01).对照组罕见AT1R表达,模型组AT1R表达明显增高,治疗组和预防组的AT1R表达较模型组减少(P＜0.01).结论门脉高压性胃病时胃血管紧张素Ⅱ1型受体表达升高,洛沙坦不仅可以降低门脉压力,而且抑制黏膜下AT1R活性,对门脉高压性胃病有治疗作用.     

福辛普利对自发性高血压左心室肥厚大鼠心肌细胞凋亡的影响

目的：探明福辛普利对伴左心室肥厚（LVH）的自发性高血压大鼠（SHR）心肌细胞凋亡的影响。方法：采用末端脱氧核糖核苷酸转移酶介导的dUTP缺口末端标记（TUNEL）技术检测SHR和WKY大鼠左心室心肌细胞凋亡变化。另外,将12只10月龄SHR随机分为两组,分别给予生理盐水（Control组）和福辛普利(Fosinopril组）腹腔内注射进行为期8周的干预治疗,以探明福辛普利对SHR的LVH和心肌细胞凋亡的影响。结果：（1）SHR组LVH指数显著高于WKY大鼠组（P＜0．01）;（2）SHR组凋亡阳性心肌细胞核数目和心肌细胞凋亡指数均显著低于WKY大鼠组（P＜0．01）;（3）SHR组心肌细胞凋亡指数与LVH指数呈显著负相关（P＜0．01）。（4)Fosinopril组LVH指数较Control组显著降低,但凋亡阳性心肌细胞核数目和心肌细胞凋亡指数较Control组显著增加（P均＜0．01）。结论：（1）SHR左心室心肌细胞凋亡不足可能在LVH发病中起重要作用。（2）Fosinopril 能显著改善SHR的LVH,其 机制之一可能与促进心肌细胞凋亡有关。