Functional coupling of angiotensin II type 1 receptor with insulin resistance of energy substrate uptakes in immortalized cardiomyocytes (HL-1 cells).

摘要: Background and purpose: Increased angiotensin II levels insulin resistance coexist at the early stages of cardiomyopathies. To determine whether increases in cardiomyocytes, we studied effect on basal insulin-stimulated transport rate energy substrates immortalized cardiomyocytes (HL-1 cells). Experimental approach: Glucose palmitic acid uptakes were measured using [3H]2-deoxy-D-glucose [14C]palmitic acid, respectively, cells exposed or not to (100 nM), plus irbesartan PD123319, type 1 2 receptor antagonists, PD98059, an inhibitor ERK1/2 activation. Cell viability, DNA, protein synthesis surface area evaluated by MTT test, [3H]thymydine, [3H]leucine morphometric analysis, respectively. Type western blot analysis. Key results: Basal glucose HL-1 (0.37±0.07 7.31±0.22 pmol per 104cells min, respectively) both stimulated 100 nM (+91 +64%, respectively). Cells remained viable did show signs hypertrophy. In these conditions, uptake increased (11.41±0.46 pmol 104 min) failed stimulate fatty acids. Changes prevented significantly reduced PD98059. Conclusions implications: Angiotensin is a candidate for increasing cardiomyocytes. Our results suggest further mechanism cardiovascular protection offered blockers. British Journal Pharmacology (2008) 153, 907–914; doi:10.1038/sj.bjp.0707563; published online 5 November 2007