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81.
ANGIOTENSIN CONVERTING ENZYME (ACE) INHIBITORS AND KININ METABOLISM: EVIDENCE THAT ACE INHIBITORS MAY INHIBIT A KININASE OTHER THAN ACE 总被引:1,自引:0,他引:1
Duncan J. Campbell 《Clinical and experimental pharmacology & physiology》1995,22(12):903-911
1. Angiotensin converting enzyme (ACE) converts angiotensin I to angiotensin II, and also metabolizes bradykinin-(1–9) to bradykinin-(1–7) and bradykinin-(1–7) to bradykinin-(1–5). Increases in endogenous kinin levels may contribute to the therapeutic effects of ACE inhibitors. 2. ACE inhibitors increase vascular levels of both bradykinin-(1–9) and its ACE cleavage product bradykinin-(1–7), at doses below the threshold for ACE inhibition, leading to the proposal that ACE inhibitors may also inhibit a non-ACE kininase which cleaves both kinin peptides; this non-ACE kininase may be the major pathway of kinin metabolism in the vasculature and some other tissues. 3. In support of this proposal, ACE inhibitors potentiate bradykinin-(1–9) effects at doses which have little or no effect on ACE activity, as indicated by angiotensin I conversion to angiotensin II. ACE inhibitors also potentiate the actions of ACE-resistant kinin analogues, which may be susceptible to metabolism by a non-ACE kininase. 4. Identification and characterization of the putative non-ACE kininase which is inhibited by ACE inhibitors may reveal novel approaches to the tissue-specific modulation of kinin levels. 相似文献
82.
基质金属蛋白酶及其抑制剂在子宫内膜癌的侵袭和转移中发挥着重要的作用。肿瘤的新生血管对肿瘤的发生、发展、转移及预后有着重要作用。微血管密度是衡量血管生成的定量指标。基质金属蛋白酶抑制剂可抑制血管的生成和MMPs对细胞外基质的降解。现将他们与子宫内膜癌的关系综述如下。 相似文献
83.
84.
目的探讨123I-MIBG心肌显像在治疗前预测依那普利对扩张型心肌病(DCM)患者治疗效果的临床价值。方法对24例DCM患者于依那普利治疗前行早期(20min)及延迟(3h)123I-MIBG心肌显像,采用心/上纵隔(H/M)比和心脏放射性洗脱率(WR)作为相对半定量计数分析,与超声心功能参数进行对比。根据123I-MI-BG心肌显像延迟相的H/M分为3组延迟H/M≥1.7为组Ⅰ,1.5<延迟H/M<1.7为组Ⅱ,延迟H/M≤1.5为组Ⅲ。组Ⅰ和组Ⅱ在平均治疗4.5个月后重复以上检查。结果治疗前3组间超声心功能参数比较均无统计学差异。治疗后组Ⅰ的左室射血分数(LVEF)和左室收缩末径(LVDs)明显改善,早期H/M和延迟H/M均明显改善(P<0.05),而WR无明显变化。治疗后组Ⅱ的延迟H/M明显改善(P<0.05),而早期H/M和WR均无明显变化,心功能参数也无改善。组Ⅰ和组Ⅱ患者均能耐受依那普利治疗,而组Ⅲ患者均不能耐受依那普利治疗。结论123I-MIBG心肌显像在治疗前预测依那普利对DCM患者的治疗效果方面有一定价值。 相似文献
85.
A M Abdel Gader A A Al-Mishari S A Awadalla N M Buyuomi T Khashoggi M Al-Hakeem 《International journal of gynaecology and obstetrics》2006,95(3):248-253
OBJECTIVE: To clarify the role played by tissue factor pathway inhibitor (TFPI) in pregnancy hypertension. METHODS: Using enzyme-linked immunosorbent assays, hemostatic measurements were obtained for women with pre-eclampsia (n=51), nonproteinuric hypertension of pregnancy (n=62), postpartum pre-eclampsia 24 h after childbirth (n=31), and no hypertension (healthy pregnant controls, n=100). RESULTS: There was a significant increase in circulating free TFPI levels in women with pre-eclampsia (9.7+/-6.2 ng/mL) or nonproteinuric hypertension of pregnancy (8.3+/-5.3 ng/mL) compared with healthy controls (5.3+/-2.1 ng/mL). In women with pre-eclampsia the levels remained elevated after placental delivery (10.6+/-4.0 ng/mL). Free protein S levels were significantly higher in women with pre-eclampsia (40.0%+/-10.7%), nonproteinuric hypertension of pregnancy (37.1%+/-12.5%), or postpartum pre-eclampsia (39.3%+/-9.1%) than in healthy pregnant controls (32.2%+/-8.5%). CONCLUSION: Increased levels of the physiologically active free forms of TFPI and free protein S, 2 coagulation inhibitors, may protect women with pregnancy-induced hypertension from the risks of hemostatic activation. 相似文献
86.
目的探讨过氧化体增殖物激活型受体α(PPARα)的特异性激活物亚油酸对HepG2细胞1型纤溶酶原激活物抑制剂(PAI-1)mRNA表达及其活性的影响和在该基因转录调控中的作用机制.方法用不同浓度亚油酸为诱导因素刺激HepG2细胞,采用半定量RT-PCR法检测PAI-1mRNA水平,发色底物法检测PAI-1的活性变化.构建四个含PAI-1启动子序列从-804~+17间不同长度片段驱动的荧光素酶报告基因质粒,体外瞬时转染HepG2细胞,检测荧光素酶的活性.结果与对照组相比,亚油酸组能使HepG2细胞PAI-1mRNA表达及蛋白活性显著升高(P<0.05,P<0.01),且呈一定剂量依赖性;亚油酸诱导可使PAI-1转录活性显著升高(P<0.01);与转染质粒PAI-pGL3-A(-804/+17)相比较,当转染质粒含有PAI-pGL3-B(-636/+17)、PAI-pGL3-C(-449/+17)时,荧光素酶活性显著降低(P<0.01);共转染PPARα表达质粒(PPARα-pSG5)的细胞在亚油酸诱导下PAI-1转录活性显著升高(P<0.01).结论亚油酸可以增加HepG2细胞PAI-1mRNA表达及其蛋白活性,调节PAI-1的基因转录,PPARα参与亚油酸对PAI-1基因的表达调控;在PAI-1启动子-804~-636、-449~-276区域内存在亚油酸作用的调控PAI-1基因表达的序列. 相似文献
87.
Summary. Patients with mild or moderate haemophilia A usually have a mild bleeding disorder requiring only occasional treatment with factor VIII (FVIII) concentrates. The frequency of inhibitor development in such patients has been the subject of several recent surveys, which significantly modified our appreciation of this complication. Studies of the anti-FVIII antibodies provided an explanation for the different bleeding phenotypes observed in mild/moderate haemophilia A patients with inhibitors. Antibodies distinguishing between the patient's mutant FVIII and the normal wild-type FVIII were characterized, in addition to antibodies inhibiting completely or only partially FVIII activity. T lymphocytes recognizing FVIII and likely involved in the development of the immune response to FVIII were successfully identified. The FVIII peptides recognized by those FVIII-specific cells bind to many major histocompatibility complex (MHC) class II molecules, which may provide an explanation for the lack of strong association between MHC haplotypes and inhibitor development. Although these studies have advanced our understanding of the conditions leading to inhibitor development, further work is required to determine whether the mode of FVIII administration significantly influences inhibitor development. Further studies of the genetic factors are also required to fully understand the mechanisms leading to inhibitor development in patients with mild/moderate haemophilia A. 相似文献
88.
89.
高脂血症对血浆t-PA和PAI-1活性的影响 总被引:2,自引:0,他引:2
目的 探讨高脂血症患者的纤溶系统的变化。方法 选取正常人及高脂血症者,测定其血脂、血浆t—PA和PAI-1活性。结果 高脂血症组比正常人血浆t—PA活性下降,而PAI-1的活性有升高;在TG及LDL-C升高者,其血浆t—PA活性比正常人血浆t—PA活性降低,而血浆PAI-1活性比正常人升高;单纯TC升高者血浆PAI-1活性接近正常人组,而血浆t—PA活性比正常人组明显降低。结论 高脂血症对纤溶系统有一定的影响,其中甘油三酯和LDL-C对纤溶系统的影响更明显,而胆固醇对纤溶系统也有一定的影响。 相似文献
90.
Alex W Wilson Stephen J Medhurst Claire I Dixon Nick C Bontoft Lisa A Winyard Kim T Brackenborough Jorge De Alba Christopher J Clarke Martin J Gunthorpe Gareth A Hicks Chas Bountra Daniel S McQueen Iain P Chessell 《European Journal of Pain》2006,10(6):537-549
Clinically, inflammatory pain is far more persistent than that typically modelled pre-clinically, with the majority of animal models focussing on short-term effects of the inflammatory pain response. The large attrition rate of compounds in the clinic which show pre-clinical efficacy suggests the need for novel models of, or approaches to, chronic inflammatory pain if novel mechanisms are to make it to the market. A model in which a more chronic inflammatory hypersensitivity phenotype is profiled may allow for a more clinically predictive tool. The aims of these studies were to characterise and validate a chronic model of inflammatory pain. We have shown that injection of a large volume of adjuvant to the intra-articular space of the rat knee results in a prolonged inflammatory pain response, compared to the response in an acute adjuvant model. Additionally, this model also results in a hypersensitive state in the presence and absence of inflammation. A range of clinically effective analgesics demonstrate activity in this chronic model, including morphine (3mg/kg, t.i.d.), dexamethasone (1mg/kg, b.i.d.), ibuprofen (30mg/kg, t.i.d.), etoricoxib (5mg/kg, b.i.d.) and rofecoxib (0.3-10mg/kg, b.i.d.). A further aim was to exemplify the utility of this chronic model over the more acute intra-plantar adjuvant model using two novel therapeutic approaches; NR2B selective NMDA receptor antagonism and iNOS inhibition. Our data shows that different effects were observed with these therapies when comparing the acute model with the model of chronic inflammatory joint pain. These data suggest that the chronic model may be more relevant to identifying mechanisms for the treatment of chronic inflammatory pain states in the clinic. 相似文献