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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, RESULTS. Meshes: Angiotensin II, Angiotensinogen, Animals, Blood Pressure, Cardiomegaly, Cells, Cultured, Enzyme Activation, Female, Hypertension, In Vitro Techniques, JNK Mitogen-Activated Protein Kinases, MAP Kinase Kinase 4, Male, Mice, Mice, Inbred C57BL, Mice, Transgenic, Mitogen-Activated Protein Kinase Kinases, Mitogen-Activated Protein Kinases, Myocardium, Myosin Heavy Chains, Promoter Regions, Genetic, Renin, Stress, Mechanical, Transgenes, Vasoconstrictor Agents, p38 Mitogen-Activated Protein Kinases.
user
Is angiotensin II-induced cardiac hypertrophy associated with different mitogen-activated protein kinase activation in normotensive and hypertensive mice? Context: 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. 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.
assistant
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. Final Decision: yes