替米沙坦与贝那普利对轻度高血压患者EL活性和APN水平的干预研究
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摘要
目的本研究旨在比较轻度原发性高血压(EH)患者与正常血压者的血清内皮脂肪酶(EL)活性和脂联素(APN)浓度,分析血清EL和APN与轻度EH患者血压的关系,并且观察轻度EH患者服用替米沙坦或贝那普利前后内皮脂肪酶(EL)活性和脂联素(APN)浓度的变化。
方法选取符合纳入标准的68例轻度EH患者和30例正常对照者,EH患者予以安慰剂(维生素B1)洗脱2周,将68例轻度EH患者采用随机,单盲的方法分为替米沙坦组34例和贝那普利组34例,分别予以口服替米沙坦40mg或贝那普利10mg,每天1次,4周后如血压未达标,则剂量加倍,疗程12周,每2周随访一次(观察患者血压,用药情况及不良反应),治疗前及治疗12周后空腹抽取外周血,用酶联免疫吸附法(ELISA)测定血清EL活性和APN浓度。
结果①正常对照组与轻度高血压组研究对象一般资料比较：除血压有明显差异外,其他各生化和生理指标比较均无差异,具有可比性。②轻度EH患者治疗前血清EL活性显著高于正常对照组：(409.11+35.35)μg/L VS(319.78+17.31)μg/L,(P<0.01)；轻度EH患者治疗前血清APN浓度显著低于正常对照组(5.13±0.59)mg/L VS(8.36+0.30)mg/L, (P<0.01)。经替米沙坦或贝那普利治疗12周后,与治疗前比较,替米沙坦组和贝那普利组血清EL活性显著降低：(411.22±35.29)μ/LVS (330.51±20.36)μg/L；(406.94±35.88)μg/LVS(357.14±27.96)μg/L,均(P<0.01)；而APN浓度显著升高：(5.13±0.57)mg/LVS(8.28±0.24)mg/L: (5.12±0.61)mg/LVS (7.51±0.81)mg/L,均(P<0.01)。替米沙坦组治疗后EL活性下降值和APN浓度升高值水平均高于贝那普利组,两组治疗前后血清EL和APN水平差值比较：80.71士18.92μg/L VS49.80±11.66μg/L；3.15±0.48 mg/L VS2.41±0.56 mg/L,均(P<0.05)。③轻度EH患者用药前后自身对比,收缩压(SBP)、舒张压(DBP)平均动脉压(MAP)下降程度均有显著差异均(P<0.01)。④经多元线性回归分析显示,轻度EH患者的血清EL与SBP.LDL呈正相关(r=0.380,P=0.002；r=0.301,P=0.017),与HDL.TC.APN浓度呈负相关(r=-0.395,P=0.001；r==-0.330,P=0.008；r:=-0.282,P=0.025).
结论①轻度EH患者血清EL活性增加而APN浓度降低。②轻度EH患者血清EL活性与SBP、LDL浓度呈正相关,与HDL、TC和APN浓度呈负相关。③替米沙坦和贝那普利均能使轻度高血压患者血清EL活性降低及APN水平升高,但替米沙坦更显优越。
Aim:To determine the activity of the endothelial lipase and the levels of adiponectin in the serum of patients with mild essential hypertension, to analyze the relationship between the activity of the endothelial lipase and adiponectin and the blood pressure of patients with mild essential hypertension, and to observe the changes of the endothelial lipase activity and adiponectin concentrations in patients with mild essential hypertension treated with telmisartan or benazepril.
Methods:68 patients with mild essential hypertension at the age of 30 to 70 were enrolled in the study. After 2 weeks of placebo treatment with the vitamin B1,68 patients were divided into two groups with 34 patients of each by single-blind method (telmisartan 40mg once a day or benazepril 5mg once a day). After 4 weeks treatment, those whose blood pressure was not well controlled were correspondently required to take telmisartan 80mg once a day and benazepril 10mg once a day. The treatment lasted 12 weeks. During this period the patients were followed once every two weeks (their blood pressure, status of medication and adverse reactions were recorded). After 12 weeks'treatment, the activity of the endothelial lipase and concentrations of adiponectin in the serum of patients were determined by ELISA (enzyme linked immune sorbent assay).
Results:①There was not obvious difference except for the difference of their blood pressure between control and hypertensive group, suggesting that data had comparability in these two groups.②Before the treatment, the activity of the endothelial lipase in the serum of patients with mild essential hypertension was greatly higher than that of control group:(409.11±35.35)μg/L vs (319.78±17.31)μg/L, (P<0.01); and the concentrations of adiponectin in the serum of patients in the hypertension group were significantly lower than those of the control group:(5.13±0.59)mg/L vs(8.36±0.30)mg/L, (P<0.01). After 12 weeks treatment of telmisartan or benazepril, the activity of endothelial lipase in patients with mild essential hypertension was markedly decreased:(411.22±35.29)μg/L vs (330.51±20.36)μg/L (406.94±35.88)μg/L vs (357.14±27.96)μg/L, respectively (P<0.01); while the levels of adiponectin in hypertensive patients were significantly increased:(5.13±0.57) mg/L vs (8.28±0.24) mg/L, (5.12±0.61) mg/L vs (7.51±0.81) mg/L, respectively (P<0.01). After the treatment, both the decrease in the endothelial lipase activity and the increase in the concentrations of the adiponectin in telmisartan group were better than those of benazepril group (80.71±18.92μg/L vs 49.80±11.66μg/L; 3.15±0.48 mg/L vs 2.41±0.56 mg/L, respectively).③The SBP (systolic blood pressure)、DBP (diastolic blood pressure) and MAP(mean arterial blood pressure) of patients with mild essential hypertension were greatly decreased after treatment with telmisartan or benazepril (P<0.01). According to the analysis of multiple linear regression, the endothelial lipase activity in patients with mild essential hypertension was positively correlated with SBP and lower-density lipoprotein cholesterol (r=0.380, P=0.002; r=0.301, P=0.017, respectively), and was negatively correlated with high-density lipoprotein cholesterol, total cholesterol and adiponectin (r=-0.395, P=0.001; r=-0.330, P=0.008; r=-0.282, P=0. 025).
Conclusion:①The activity of the endothelial lipase was increased and the concentrations of the adiponectin were decreased in patients with mild essential hypertension.②The activity of the endothelial lipase in patients with essential hypertension was positively correlated with systolic blood pressure and lower-density lipoprotein cholesterol, and was negatively correlated with their high-density lipoprotein cholesterol, total cholesterol and adiponectin.③Both of telmisartan and benazepril could decrease the endothelial lipase activity and increase the adiponectin levels in patients with mild essential hypertension, but telmisartan had better effects.
方法选取符合纳入标准的68例轻度EH患者和30例正常对照者,EH患者予以安慰剂(维生素B1)洗脱2周,将68例轻度EH患者采用随机,单盲的方法分为替米沙坦组34例和贝那普利组34例,分别予以口服替米沙坦40mg或贝那普利10mg,每天1次,4周后如血压未达标,则剂量加倍,疗程12周,每2周随访一次(观察患者血压,用药情况及不良反应),治疗前及治疗12周后空腹抽取外周血,用酶联免疫吸附法(ELISA)测定血清EL活性和APN浓度。
结果①正常对照组与轻度高血压组研究对象一般资料比较：除血压有明显差异外,其他各生化和生理指标比较均无差异,具有可比性。②轻度EH患者治疗前血清EL活性显著高于正常对照组：(409.11+35.35)μg/L VS(319.78+17.31)μg/L,(P<0.01)；轻度EH患者治疗前血清APN浓度显著低于正常对照组(5.13±0.59)mg/L VS(8.36+0.30)mg/L, (P<0.01)。经替米沙坦或贝那普利治疗12周后,与治疗前比较,替米沙坦组和贝那普利组血清EL活性显著降低：(411.22±35.29)μ/LVS (330.51±20.36)μg/L；(406.94±35.88)μg/LVS(357.14±27.96)μg/L,均(P<0.01)；而APN浓度显著升高：(5.13±0.57)mg/LVS(8.28±0.24)mg/L: (5.12±0.61)mg/LVS (7.51±0.81)mg/L,均(P<0.01)。替米沙坦组治疗后EL活性下降值和APN浓度升高值水平均高于贝那普利组,两组治疗前后血清EL和APN水平差值比较：80.71士18.92μg/L VS49.80±11.66μg/L；3.15±0.48 mg/L VS2.41±0.56 mg/L,均(P<0.05)。③轻度EH患者用药前后自身对比,收缩压(SBP)、舒张压(DBP)平均动脉压(MAP)下降程度均有显著差异均(P<0.01)。④经多元线性回归分析显示,轻度EH患者的血清EL与SBP.LDL呈正相关(r=0.380,P=0.002；r=0.301,P=0.017),与HDL.TC.APN浓度呈负相关(r=-0.395,P=0.001；r==-0.330,P=0.008；r:=-0.282,P=0.025).
结论①轻度EH患者血清EL活性增加而APN浓度降低。②轻度EH患者血清EL活性与SBP、LDL浓度呈正相关,与HDL、TC和APN浓度呈负相关。③替米沙坦和贝那普利均能使轻度高血压患者血清EL活性降低及APN水平升高,但替米沙坦更显优越。
Aim:To determine the activity of the endothelial lipase and the levels of adiponectin in the serum of patients with mild essential hypertension, to analyze the relationship between the activity of the endothelial lipase and adiponectin and the blood pressure of patients with mild essential hypertension, and to observe the changes of the endothelial lipase activity and adiponectin concentrations in patients with mild essential hypertension treated with telmisartan or benazepril.
Methods:68 patients with mild essential hypertension at the age of 30 to 70 were enrolled in the study. After 2 weeks of placebo treatment with the vitamin B1,68 patients were divided into two groups with 34 patients of each by single-blind method (telmisartan 40mg once a day or benazepril 5mg once a day). After 4 weeks treatment, those whose blood pressure was not well controlled were correspondently required to take telmisartan 80mg once a day and benazepril 10mg once a day. The treatment lasted 12 weeks. During this period the patients were followed once every two weeks (their blood pressure, status of medication and adverse reactions were recorded). After 12 weeks'treatment, the activity of the endothelial lipase and concentrations of adiponectin in the serum of patients were determined by ELISA (enzyme linked immune sorbent assay).
Results:①There was not obvious difference except for the difference of their blood pressure between control and hypertensive group, suggesting that data had comparability in these two groups.②Before the treatment, the activity of the endothelial lipase in the serum of patients with mild essential hypertension was greatly higher than that of control group:(409.11±35.35)μg/L vs (319.78±17.31)μg/L, (P<0.01); and the concentrations of adiponectin in the serum of patients in the hypertension group were significantly lower than those of the control group:(5.13±0.59)mg/L vs(8.36±0.30)mg/L, (P<0.01). After 12 weeks treatment of telmisartan or benazepril, the activity of endothelial lipase in patients with mild essential hypertension was markedly decreased:(411.22±35.29)μg/L vs (330.51±20.36)μg/L (406.94±35.88)μg/L vs (357.14±27.96)μg/L, respectively (P<0.01); while the levels of adiponectin in hypertensive patients were significantly increased:(5.13±0.57) mg/L vs (8.28±0.24) mg/L, (5.12±0.61) mg/L vs (7.51±0.81) mg/L, respectively (P<0.01). After the treatment, both the decrease in the endothelial lipase activity and the increase in the concentrations of the adiponectin in telmisartan group were better than those of benazepril group (80.71±18.92μg/L vs 49.80±11.66μg/L; 3.15±0.48 mg/L vs 2.41±0.56 mg/L, respectively).③The SBP (systolic blood pressure)、DBP (diastolic blood pressure) and MAP(mean arterial blood pressure) of patients with mild essential hypertension were greatly decreased after treatment with telmisartan or benazepril (P<0.01). According to the analysis of multiple linear regression, the endothelial lipase activity in patients with mild essential hypertension was positively correlated with SBP and lower-density lipoprotein cholesterol (r=0.380, P=0.002; r=0.301, P=0.017, respectively), and was negatively correlated with high-density lipoprotein cholesterol, total cholesterol and adiponectin (r=-0.395, P=0.001; r=-0.330, P=0.008; r=-0.282, P=0. 025).
Conclusion:①The activity of the endothelial lipase was increased and the concentrations of the adiponectin were decreased in patients with mild essential hypertension.②The activity of the endothelial lipase in patients with essential hypertension was positively correlated with systolic blood pressure and lower-density lipoprotein cholesterol, and was negatively correlated with their high-density lipoprotein cholesterol, total cholesterol and adiponectin.③Both of telmisartan and benazepril could decrease the endothelial lipase activity and increase the adiponectin levels in patients with mild essential hypertension, but telmisartan had better effects.
引文
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[1]Hirata K, Dichek HL, cioffi JA, et al. Cloning of a unique lipase from endothelial cells extends the lipase gene family[J]. Biol chem,1999,274(20): 14170-14175.
[2]Jaye M, Lynch KJ, Krawiec J, et al. A novel endothelial-derived lipase that modulates HDL metabolism [J]. Nat Genet,1999,21(4):424-428.
[3]Azumi H, Hirata K, Ishida T, et al. Immunohistochemical localization of endothelial cell-derived lipase in atherosclerotic human coronary arteries [J]. Cardiovasc Res,2003,58(3):647-654.
[4]Badellino KO, Wolfe ML, Reilly MP, et al. Endothelial lipase concentrations are increased in metabolic syndrome and associated with coronary atherosclerosis [J]. PLOS Med,2006,3(2):e22.
[5]Ishida T, Choi S, Kundu RK, et al. Endothelial lipase is a major determinant of HDL level[J]. J Clin Invest,2003, 111(3):347-355.
[6]Mccoy MG, Sun GS, Marchadier D, et al. Characterization of the lipolytic activity of endothelial lipase[J]. J Lipid Res,2002,43(6):921-929.
[7]Broedl UC, Jin W, Marchadier D, et al. Tissue-specific expression pattern of human endothelial lipase in transgenic mice [J]. Atherosclerosis,2005,181 (2): 271-274.
[8]Jin WJ, Wang X, Millar JS, et al. Hepatic proprotein connvertases modulate HDL metabolism [J]. Cell Mtab,2007,6(2):129-136.
[9]Kratky D, Zimmermann R, Wagner EM, et al. Endothelial lipase provides an alternative pathway for FFA uptake in lipoprotein lipase-deficient mouse adipose tissue[J]. J Clin Invest 2005,115(1):161-167.
[10]Jin W, Millar JS, Broedl U, et al. Inhibition of endothelial lipase causes increased HDL cholesterol levels in vivo[J]. Clin Invest,2003,111(3):357-362.
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[1]Hirata K, Dichek HL, cioffi JA, et al. Cloning of a unique lipase from endothelial cells extends the lipase gene family[J]. Biol chem,1999,274(20): 14170-14175.
[2]Jaye M, Lynch KJ, Krawiec J, et al. A novel endothelial-derived lipase that modulates HDL metabolism [J]. Nat Genet,1999,21(4):424-428.
[3]Azumi H, Hirata K, Ishida T, et al. Immunohistochemical localization of endothelial cell-derived lipase in atherosclerotic human coronary arteries [J]. Cardiovasc Res,2003,58(3):647-654.
[4]Badellino KO, Wolfe ML, Reilly MP, et al. Endothelial lipase concentrations are increased in metabolic syndrome and associated with coronary atherosclerosis [J]. PLOS Med,2006,3(2):e22.
[5]Ishida T, Choi S, Kundu RK, et al. Endothelial lipase is a major determinant of HDL level[J]. J Clin Invest,2003, 111(3):347-355.
[6]Mccoy MG, Sun GS, Marchadier D, et al. Characterization of the lipolytic activity of endothelial lipase[J]. J Lipid Res,2002,43(6):921-929.
[7]Broedl UC, Jin W, Marchadier D, et al. Tissue-specific expression pattern of human endothelial lipase in transgenic mice [J]. Atherosclerosis,2005,181 (2): 271-274.
[8]Jin WJ, Wang X, Millar JS, et al. Hepatic proprotein connvertases modulate HDL metabolism [J]. Cell Mtab,2007,6(2):129-136.
[9]Kratky D, Zimmermann R, Wagner EM, et al. Endothelial lipase provides an alternative pathway for FFA uptake in lipoprotein lipase-deficient mouse adipose tissue[J]. J Clin Invest 2005,115(1):161-167.
[10]Jin W, Millar JS, Broedl U, et al. Inhibition of endothelial lipase causes increased HDL cholesterol levels in vivo[J]. Clin Invest,2003,111(3):357-362.
[11]Skropeta D, Settasatian C,Mcmahon MR, et al. N-glycosylation regulates endothelial lipase-mediated phospholipid hydrolysis in apoE and apoAI-containing high density lipoproteins[J]. Lipid Res,2007,48(9): 2047-2057.
[12]Ahmed W, Orasanu G, Nehra V, et al. High density lipoprotein hydrolysis by endothelial lipase activates PPAR alpha:a candidate mechanism for high density lipoprotein mediated repression of leukocyte adhesion[J], Circ Res,2006, 98(4):490-498.
[13]Broedl UC, Maugeais C, Marchadier D, et al. Effects of nonlipolytic ligand function of endothelial lipase on HDL metabolism in vivo[J].Biol Chem,2003, 278(42):40688-40693.
[14]Delemos AS, Wolfe ML, Long CJ, et al.Indentification of genetic variants in endothelial lipase in persons with elevatedhigh density lipoproteins cholesterol [J].Circulation,2002,106(11):321-326.
[15]Yamakawa-kobayashi K, Yanagi H,Endo K,et al. Relationship between serum HDL-C levels and common genetic variants of the endothelial lipase gene in Japancse school-age children[J].Hum Genet,2003,113(4):311-315.
[16]Maric-Eve Paradis, Patrick Couture, Yohan Bosst, et al. The T111I mutation in the endothelial lipase gene modulates the impact of dietary fat on the HDL profile in women[J].Lipid Res,2003,44(10):1902-1908.
[17]马天容,潘其兴,朱清,等.阿托伐他汀对内皮细胞增值和内皮脂酶mRNA表达的影响[J].中国动脉硬化杂志。2006,14(6)：471-474.
[18]范乐明.动脉粥样硬化炎症机制的再认识[J].中国动脉硬化杂志,2005,13(3)：249-253.
[19]Hirata K, Ishida T, Matsushita H, et al. Regulated expression of endothelial cellderived lipase[J]. Biochem Biophys Res Commun,2000,272(1):90-93.
[20]Jin W, Sun GS, Marchadier D, et al. Endothelial cells secrete triglyceride lipase and phospholipase activities in response to cytokines as a result of endothelial lipase[J]. circ Res.2003,92(6):644-650.
[21]Badellino KO, Wolfe ML, Reilly MP, et al. Endothelial lipase is increased in vivo by inflammation in humans[J].Circulation,2008,117(5):678-685.
[22]Paradis ME, Badellino KO, Rader DJ, et al. Endothelial lipase is associated with inflammation in humans[J].Lipid Res,2006,47(12):2808-2813.
[23]Wang X, Jin W, Dader DJ, et al. Upregulation of macrophage endothelial lipase by toll-like receptors 4 and 3 modulates macrophage interleukin-10 and-12 production [J]. Circ Res,2007,100(7):1008-1015.
[24]Das UN. Long-chain polyunsaturated fatty acids, endothelial lipase and atherosclerosis [J]. Prostaglandins Leukot Essent Fatty Acids,2005,72(3): 173-179.
[25]Fuki IV, Blanchard N, Jin WJ, et al. Endogenously produced endothelial lipase enhances binding and cellular processing of plasma lipoproteins via heparan sulfate proteoglycan-mediated pathway [J]. J Biol Chem,2003,278(36): 34331-34338.
[26]Hasham SN, Pillarisetti S. Vascular lipases, Inflammation and atherosclerosis [J]. Clin Chim Acta,2006,372(1-2):179-183.
[27]成丽英,边云飞,杨晓静,等.冠心病危险因素对内皮脂肪酶表达的影响作用[J].中国分子心脏病学杂志,2008,8(1)：17-20.
[28]Ozaki K, Ohnishi Y, Iida A, et al. Functional SNPS in the lymphotoxin-alpha gene that are associated with susceptibility to myocardial infarction[J]. Nature Genetics,2002,32(4):650-654.
[29]方玉强,黄岚,李爱民,等.冠心病患者循环内皮细胞内皮脂肪酶表达与冠脉危险积分的关系及意义[J].中国急救医学,2008,28(1)：5-8.
[30]Hutter CM, Austin MA, Farin FM, et al. Association of endothelial lipase gene(LIPG) haplotypes with high density lipoprotein cholesterol subfractions and apolipoprotein AI plasma levels in Japanese Americans [J]. Atherosclerosis, 2006,185(1):78-86.
[31]Shimizu M, Kanazawa K, Hirata K, et al. Endothelial lipase gene polymorphism is associated with acute myocardial infarction,independently of high-density lipoprotein-cholesterol levels[J]. Circ J,2007,71(6):842-846.
[32]成丽英,边云飞,杨晓静,等.内皮脂肪酶与冠心病的相关性研究[J].中国心血管杂志,2008,13(1)：15-20.
[33]Kearney PM, Whelton M, Reynolds K, et al. Global burden of hypertension: analysis of worldwide data[J]. Lancet,2005,365(9455):217-223.
[34]Hirseh AT. Vascular disease, Hypertension and prevention:From endothelium to clinical events[J]. JACC,2003,42(2):377-379.
[35]Jahangiri A, Rader DJ, Marchadier D, et al. Evidence that endothelial lipase remodels high density lipoproteins without mediating the dissociation of apolipo-protein A-I[J]. J Lipid Res,2005,46(7):896-903.
[36]Shimokawa Y, Hirata K, Ishida T, et al. Increased expression of endothelial lipase in rat models of hypertension[J]. Cardiovase Res,2005,66(3):594-600.
[37]杨晓静,边云飞,成丽英,等.内皮脂肪酶与原发性高血压的相关性研究[J].中西医结合心脑血管病杂,2008,6(6)：671-673.
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