AGT and hypertensive disorder: We established that: (1) Raf paradox signalling induced by dabrafenib in cardiac cells is limited; (2) dabrafenib inhibits ERK1/2 activity in isolated cardiac cells, in ex vivo perfused adult rat hearts and in a murine model of hypertension induced by angiotensin II (AngII); and (3), inhibition of Raf kinases with dabrafenib reduced cardiomyocyte hypertrophy, cardiac inflammation and cardiac fibrosis induced by AngII in both acute (7 d) and chronic (28 d) treatment conditions.