ALPHA-ADRENERGIC AND BETA-ADRENERGIC STIMULATION OF PROTEIN-SYNTHESIS IN CULTURED ADULT VENTRICULAR CARDIOMYOCYTES

被引:82
作者
PINSON, A
SCHLUTER, KD
ZHOU, XJ
SCHWARTZ, P
KESSLERICEKSON, G
PIPER, HM
机构
[1] UNIV DUSSELDORF, INST PHYSIOL 1, MOORENSTR 5, W-4000 DUSSELDORF 1, GERMANY
[2] HEBREW UNIV JERUSALEM, HADASSAH MED SCH, INST BIOCHEM, MYOCARDIAL RES LAB, IL-91010 JERUSALEM, ISRAEL
[3] UNIV GOTTINGEN, ZENTRUM ANAT, W-3400 GOTTINGEN, GERMANY
[4] BEILINSON MED CTR, ROGOFF MED RES INST, IL-49100 PETAH TIQWA, ISRAEL
关键词
ALPHA(1)-ADRENERGIC RECEPTOR; BETA-ADRENERGIC RECEPTOR; MYOCARDIAL HYPERTROPHY; CREATINE KINASE; PROTEIN SYNTHESIS; RNA SYNTHESIS; ISOLATED CARDIOMYOCYTES;
D O I
10.1006/jmcc.1993.1053
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The effect of the α1-adrenoceptor agonist phenylephrine (PE, 1-10 μM) and the β-adrenoceptor agonist isoprenaline (ISO, 1-10 μM) on protein synthesis and ultrastructure of ventricular cardiomyocytes from adult rat in culture (6 days in medium 199 plus 20% fetal calf serum) was studied. In these cultures cardiomyocytes were spread, but not spontaneously contractile. ISO and PE significantly increased total cell protein and incorporation of (14C)-phenylalanine within 24 h of exposure. These effects were inhibited by the antagonists propranolol and prazosin, respectively. The incorporation of (14C)-uridine was stimulated only by PE but not ISO. Induction of fetal BB-isoform of cytosolic creatine kinase was also caused only by P.E. but not ISO. The ultrastructure of PE-treated cardiomyocytes was altered as compared to controls, by a greater number of Golgi complexes, denser myofibrillar structures and the appearance of paracrystalline hands in mitochondrial matrices. In conclusion, in this culture model protein synthesis of cardiomyocytes can be stimulated, independently of the contractility, by either α1- or β-adrenoceptor agonists. Catecholamines differ, however, in their effects on specific cellular proteins and structures. Only α1-adrenergic stimulation leads to a "fetal shift" in the expression of CK-isofoms. © 1993 Academic Press Limited.
引用
收藏
页码:477 / 490
页数:14
相关论文
共 45 条
[41]   Beta-adrenergic signals regulate cardiac differentiation of mouse embryonic stem cells via mitogen-activated protein kinase pathways [J].
Yan, Lihui ;
Jia, Zhuqing ;
Cui, Jingjing ;
Yang, Hongtao ;
Yang, Huangtian ;
Zhang, Yongzhen ;
Zhou, Chunyan .
DEVELOPMENT GROWTH & DIFFERENTIATION, 2011, 53 (06) :772-779
[42]   β-adrenergic stimulation of rat cardiac fibroblasts promotes protein synthesis via the activation of phosphatidylinositol 3-kinase [J].
Colombo, F ;
Noël, J ;
Mayers, P ;
Mercier, I ;
Calderone, A .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2001, 33 (06) :1091-1106
[43]   Ca2+-independent protein kinase C activity is required for α1-adrenergic-receptor-mediated regulation of ribosomal protein S6 kinases in adult cardiomyocytes [J].
Wang, LJ ;
Rolfe, M ;
Proud, CG .
BIOCHEMICAL JOURNAL, 2003, 373 :603-611
[44]   THE CARDIAC BETA-MYOSIN HEAVY-CHAIN ISOGENE IS INDUCED SELECTIVELY IN ALPHA-1-ADRENERGIC RECEPTOR-STIMULATED HYPERTROPHY OF CULTURED RAT-HEART MYOCYTES [J].
WASPE, LE ;
ORDAHL, CP ;
SIMPSON, PC .
JOURNAL OF CLINICAL INVESTIGATION, 1990, 85 (04) :1206-1214
[45]   STUDIES ON THE POSSIBLE ROLE OF VITREOUS-HUMOR ON PROTEIN-SYNTHESIS AND MORPHOLOGY OF ORGAN CULTURED ADULT-RABBIT LENS .2. EPITHELIAL-CELLS [J].
BANERJEE, A ;
RICHIERT, DM ;
EMANUEL, K ;
SINGH, AK ;
BAGCHI, M .
BIOCHIMICA ET BIOPHYSICA ACTA, 1991, 1076 (03) :330-336