Chymase is activated in the hamster heart following ventricular fibrosis during the chronic stage of hypertension

被引:56
作者
Shiota, N
Jin, D
Takai, S
Kawamura, T
Koyama, M
Nakamura, N
Miyazaki, M
机构
[1] Dept. Pharmacol. of Osaka Med. Coll., Takatsuki, Osaka 569
关键词
angiotensin-converting enzyme; chymase; fibrosis; apoptosis; pressure overload;
D O I
10.1016/S0014-5793(97)00295-0
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Chronic pressure overload induces cardiac tissue remodeling. Chymase is known to regulate matrix metabolism and angiotensin II formation, In the present study, we investigated the pathophysiological functions of chymase in the pressure-overloaded hamster heart induced by a two-kidney, one-clip (2K1C) hypertension procedure, Fibrosis and apoptosis were observed in the pressure-overloaded hearts of 2K1C hamsters 32 weeks after clipping, but these histological changes were not detected at 16 weeks, Heart chymase-like activity of 2K1C hamsters at 32 weeks increased 5.2-fold compared with that at 16 weeks, while angiotensin-converting enzyme was not activated, Chymase might be involved in cardiac tissue remodeling during the chronic stage of hypertension. (C) 1997 Federation of European Biochemical Societies.
引用
收藏
页码:301 / 304
页数:4
相关论文
共 33 条
[1]   THE C-MYC PROTEIN INDUCES CELL-CYCLE PROGRESSION AND APOPTOSIS THROUGH DIMERIZATION WITH MAX [J].
AMATI, B ;
LITTLEWOOD, TD ;
EVAN, GI ;
LAND, H .
EMBO JOURNAL, 1993, 12 (13) :5083-5087
[2]   THE EFFECT OF MAST-CELL CHYMASE ON EXTRACELLULAR-MATRIX - STUDIES IN AUTOIMMUNE-THYROIDITIS AND IN CULTURED THYROID-CELLS [J].
BANOVAC, K ;
DEFORTEZA, R .
INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY, 1992, 99 (01) :141-149
[3]  
BANOVAC K, 1993, P SOC EXP BIOL MED, V203, P221
[4]   HYPOTHESIS - APOPTOSIS MAY BE A MECHANISM FOR THE TRANSITION TO HEART-FAILURE WITH CHRONIC PRESSURE-OVERLOAD [J].
BING, OHL .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1994, 26 (08) :943-948
[5]   The ageing spontaneously hypertensive rat as a model of the transition from stable compensated hypertrophy to heart failure [J].
Boluyt, MO ;
Bing, OHL ;
Lakatta, EG .
EUROPEAN HEART JOURNAL, 1995, 16 :19-30
[6]  
BRAUNWALD E, 1992, HEART DISEASE TXB CA
[7]   REGULATION OF THE STRUCTURAL REMODELING OF THE MYOCARDIUM - FROM HYPERTROPHY TO HEART-FAILURE [J].
BRILLA, CG ;
MAISCH, B .
EUROPEAN HEART JOURNAL, 1994, 15 :45-52
[8]   COLLAGEN-METABOLISM IN CULTURED ADULT-RAT CARDIAC FIBROBLASTS - RESPONSE TO ANGIOTENSIN-II AND ALDOSTERONE [J].
BRILLA, CG ;
ZHOU, GP ;
MATSUBARA, L ;
WEBER, KT .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1994, 26 (07) :809-820
[9]   CASCADE INDUCTION OF C-FOS, C-MYC, AND HEAT-SHOCK 70K TRANSCRIPTS DURING REGRESSION OF THE RAT VENTRAL PROSTATE-GLAND [J].
BUTTYAN, R ;
ZAKERI, Z ;
LOCKSHIN, R ;
WOLGEMUTH, D .
MOLECULAR ENDOCRINOLOGY, 1988, 2 (07) :650-657
[10]  
CAUGHEY GH, 1988, J PHARMACOL EXP THER, V244, P133