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- W3142429470 abstract "Objective To investigate the relationship between MKP 1 and MAPK and the effect of TCV 116, an AT 1 receptor antagonist, on the changes of MAPK and MKP 1 in myocardial hypertrophy of renovascular hypertensive rats (RHR). Methods ①Two kidney and one clip renal hypertensive model was established in Sprague Dawley rats by chronic partial occlusion of left renal artery; ② Left ventricular mass to body mass ratio was measured to assay the degree of myocardial hypertrophy; ③ MAPK activity was examined using an in gel kinase assay, MKP 1 protein expression was detected by western blotting. Results ① Blood pressure, left ventricular mass to body mass ratio, MAPK activity in myocardium of RHR were increased gradually, but the increment of MKP 1 protein expression tended to dropping from 8th to 16th week after renovascular constriction. ② There was a significantly positive correlation between MAPK activity and myocardial hypertrophy, but a significantly negative correlation between MAPK activity and MKP 1 protein expression. ③ TCV116 effectively inhibited myocardial hypertrophy and prevented changes of MAPK activity and MKP 1 protein expression in RHR. Conclusion Angiotensin Ⅱ is an important factor in myocardial hypertrophy in RHR, which mediates the hypertrophic responses and activation of MAPK mainly through AT 1 receptor. The MAPK pathway is important for the development and intensification of myocardial hypertrophy by the long term activation of MAPK, and the regulation of MKP 1 on MAPK may play an important role in the development of myocardial hypertrophy in RHR." @default.
- W3142429470 created "2021-04-13" @default.
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- W3142429470 date "2000-01-01" @default.
- W3142429470 modified "2023-09-25" @default.
- W3142429470 title "The Change of MKP-1 and MAPK in Myocardium of Renovascular Hypertensive Rats" @default.
- W3142429470 hasPublicationYear "2000" @default.
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