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高血压大鼠心脏和血管丝裂素活化蛋白激酶与其磷酸酶-1的表达 被引量:4

The Changes of Mitogen-Activated Protein Kinase and Mitogen-Activated Protein Kinase Phosphatase-1 in Cardiac and Vascular Smooth Muscles of Hypertensive Rats
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摘要 目的 :探讨MAPK与MKP 1在高血压心血管重塑中的可能作用。方法 :应用Western blot的方法观察了自发性高血压大鼠(SHR)及WKY大鼠心脏和血管丝裂素活化蛋白激酶及丝裂素活化蛋白激酶磷酸酶表达的改变。结果 :(1)WKY大鼠心脏中未见有丝裂素活化蛋白激酶的表达 ,而SHR心脏中检测到了丝裂素活化蛋白激酶的表达 ;并且SHR血管中丝裂素活化蛋白激酶的表达较WKY大鼠增强90 % (P <0 0 1) ;(2 )SHR心脏及血管中丝裂素活化蛋白激酶磷酸酶 - 1的表达较WKY大鼠分别降低 5 3%及 45 % (P均<0 0 1)。结论 :SHR心脏和血管重塑的发生除与丝裂素活化蛋白激酶表达增强有关外 ,可能还与丝裂素活化蛋白激酶磷酸酶 - 1的表达下降有关。 Aim: The purpose of this study is to investigate the expression of mitogen activated protein kinase and mitogen activated protein kinase phosphatase 1 in cardiac and vascular smooth muscles of SHR. Methods:The expression of mitogen activated protein kinase and mitogen activated protein kinase phosphatase 1 were studied by Western blot. Results:The expression of mitogen activated protein kinase and mitogen activated protein kinase phosphatase 1 were found in cardiac muscles of SHR, but not in cardiac muscle of WKY rat. Meanwhile,the expression of mitogen activated protein kinase in vascular smooth muscles of SHR was 108% higher than that of WKY rat ( \%P\%< 0 01). Mitogen activated protein kinase phosphatase 1 expression in cardiac and vascular smooth muscles of SHR was marked decreased by 53% and 45% (all \%P\%< 0 01), compared with WKY rat. Conclusions:The results suggested that the remodelling of cardiac and vascular smooth muscles in SHR might be related to the increased expression of mitogen activated protein kinase and the decreased expression of mitogen activated protein kinase phosphatase 1.
出处 《高血压杂志》 CSCD 2000年第4期343-345,共3页 Chinese Journal of Hypertension
基金 国家自然科学基金资助课题!No 39970 2 95
关键词 高血压 丝裂素活化蛋白激酶 AMPK 治疗 hypertension mitogen activated protein kinase mitogen activated protein kinase phosphatase 1
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  • 1王福文,徐淑兰,崔希云.自发性高血压大鼠血管平滑肌膜电位和高血压病[J].生物医学工程研究,1999,20(3):59-62. 被引量:1
  • 2王华军,谢良地,晋学庆,陈达光.自发性高血压大鼠左心室肥厚与血压、心肌局部血管紧张素Ⅱ的关系[J].中国实验动物学杂志,1999,9(3):133-136. 被引量:7
  • 3李田昌,庞永政,苏静怡,唐朝枢.丝裂素活化蛋白激酶活性测定[J].基础医学与临床,1996,16(2):78-80. 被引量:64
  • 4李淑敏,胡大一,汪丽蕙,郑卫,庞永正,苏静怡,唐朝枢.高血压心肌肥大大鼠心肌丝裂素活化蛋白激酶的活性[J].北京医科大学学报,1996,28(3):199-201. 被引量:8
  • 5[21]Sodoshima J, Qiu Z, Morgan JP, et al. Angiotensin Ⅱ and other hypertropic stimuli mediated by G proteincoupled receptors activate tyrosine kinase, mitogen - activated protein kinase, and 90 - kD S6kinaes.Circ Res,1995,76(1):1~15
  • 6[2]Momtaz A, Coulombe A, Richer P, et al. Action potential and plate au ionic currents in moderately and severely DOCA - salt hypertrophied rat hearts.Mol Cell eardiol, 1996,28(12) :2511 ~ 2522
  • 7[4]Hu WY, Chen SC, et al. Effect of chronic captopril treatment on circulating and tissue renin angiotensin system. Acta Pharm Sinica, 1996,17(6) :507 ~ 512
  • 8[6]汤键主编.原癌基因与心血管疾病.北京:北京医学大学中国协和医院联合出版社,1990:112
  • 9[7]Wagner M, Mascareno E, Siddiqui MA Cardiac hypertrophy: signal transduction, transcriptional adaptation, and altered growth control.Annals of the New York Academy of Science, 1999,874(2): 1 ~ 10
  • 10[8]Yamazaki T, Yazaki Y. Molecular basis of cardiac hypertrophy. Z Kardiol,2000,89(1):1 ~6

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