PMID- 10994762
OWN - NLM
STAT- MEDLINE
DCOM- 20010118
LR  - 20190822
IS  - 0263-6352 (Print)
IS  - 0263-6352 (Linking)
VI  - 18
IP  - 9
DP  - 2000 Sep
TI  - Angiotensin II-induced cardiac hypertrophy is associated with different 
      mitogen-activated protein kinase activation in normotensive and hypertensive 
      mice.
PG  - 1307-17
AB  - OBJECTIVE: In addition to its haemodynamic effects, angiotensin II (AngII) is 
      thought to contribute to the development of cardiac hypertrophy via its growth 
      factor properties. The activation of mitogen-activated protein kinases (MAPK) is 
      crucial for stimulating cardiac growth. Therefore, the present study aimed to 
      determine whether the trophic effects of AngII and the AngII-induced haemodynamic 
      load were associated with specific cardiac MAPK pathways during the development 
      of hypertrophy. Methods The activation of the extracellular-signal-regulated 
      kinase (ERK), the c-jun N-terminal kinase (JNK) and the p38 kinase was followed 
      in the heart of normotensive and hypertensive transgenic mice with AngII-mediated 
      cardiac hypertrophy. Secondly, we used physiological models of AngII-dependent 
      and AngII-independent renovascular hypertension to study the activation of 
      cardiac MAPK pathways during the development of hypertrophy. RESULTS: In 
      normotensive transgenic animals with AngII-induced cardiac hypertrophy, p38 
      activation is associated with the development of hypertrophy while ERK and JNK 
      are modestly stimulated. In hypertensive transgenic mice, further activation of 
      ERK and JNK is observed. Moreover, in the AngII-independent model of renovascular 
      hypertension and cardiac hypertrophy, p38 is not activated while ERK and JNK are 
      strongly stimulated. In contrast, in the AngII-dependent model, all three kinases 
      are stimulated. CONCLUSIONS: These data suggest that p38 activation is 
      preferentially associated with the direct effects of AngII on cardiac cells, 
      whereas stimulation of ERK and JNK occurs in association with AngII-induced 
      mechanical stress.
FAU - Pellieux, C
AU  - Pellieux C
AD  - Division of Hypertension, University of Lausanne Medical School, Switzerland.
FAU - Sauthier, T
AU  - Sauthier T
FAU - Aubert, J F
AU  - Aubert JF
FAU - Brunner, H R
AU  - Brunner HR
FAU - Pedrazzini, T
AU  - Pedrazzini T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - J Hypertens
JT  - Journal of hypertension
JID - 8306882
RN  - 0 (Vasoconstrictor Agents)
RN  - 11002-13-4 (Angiotensinogen)
RN  - 11128-99-7 (Angiotensin II)
RN  - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
RN  - EC 2.7.12.2 (MAP Kinase Kinase 4)
RN  - EC 2.7.12.2 (Mitogen-Activated Protein Kinase Kinases)
RN  - EC 3.4.23.15 (Renin)
RN  - EC 3.6.4.1 (Myosin Heavy Chains)
SB  - IM
MH  - Angiotensin II/*pharmacology
MH  - Angiotensinogen/genetics
MH  - Animals
MH  - Blood Pressure
MH  - Cardiomegaly/*chemically induced/*metabolism/physiopathology
MH  - Cells, Cultured
MH  - Enzyme Activation/physiology
MH  - Female
MH  - Hypertension/*metabolism
MH  - In Vitro Techniques
MH  - *JNK Mitogen-Activated Protein Kinases
MH  - MAP Kinase Kinase 4
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Transgenic
MH  - Mitogen-Activated Protein Kinase Kinases/metabolism
MH  - Mitogen-Activated Protein Kinases/*metabolism
MH  - Myocardium/cytology/enzymology
MH  - Myosin Heavy Chains/genetics
MH  - Promoter Regions, Genetic
MH  - Renin/genetics
MH  - Stress, Mechanical
MH  - Transgenes/physiology
MH  - Vasoconstrictor Agents/*pharmacology
MH  - p38 Mitogen-Activated Protein Kinases
EDAT- 2000/09/20 11:00
MHDA- 2001/02/28 10:01
CRDT- 2000/09/20 11:00
PHST- 2000/09/20 11:00 [pubmed]
PHST- 2001/02/28 10:01 [medline]
PHST- 2000/09/20 11:00 [entrez]
AID - 10.1097/00004872-200018090-00017 [doi]
PST - ppublish
SO  - J Hypertens. 2000 Sep;18(9):1307-17. doi: 10.1097/00004872-200018090-00017.