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Am J Physiol Heart Circ Physiol 283: H768-H775, 2002. First published April 11, 2002; doi:10.1152/ajpheart.00826.2001
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Vol. 283, Issue 2, H768-H775, August 2002

Simvastatin restores endothelial NO-mediated vasorelaxation in large arteries after myocardial infarction

Kathryn Bates, Charles E. Ruggeroli, Steven Goldman, and Mohamed A. Gaballa

Cardiology Section, Southern Arizona Veterans Administration Health Care System, Tucson 85723; and Sarver Heart Center, University of Arizona, Tucson, Arizona 85724

Congestive heart failure (CHF) after myocardial infarction is associated with diminished endothelial nitric oxide (NO)-mediated vasorelaxation. The 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors have been shown to modulate vascular tone independent of the effects on lipid lowering. We hypothesized that simvastatin restores NO-dependent vasorelaxation with CHF. We found that incubation of the normal rat aorta with 0.1 mM simvastatin for 24 h enhanced ACh-mediated vasorelaxation (P < 0.05). Moreover, simvastatin increased (P < 0.05) endothelial NO synthase (eNOS) protein content by >200% (82.0 ± 14.0 vs. 21.6 ± 7.9% II/µg). In cultured endothelial cells, simvastatin (10 and 20 µM) increased eNOS levels by 114.7 ± 39.9 and 212.0 ± 75.0% II/µg protein, respectively (both P < 0.05; n = 8). In the rat coronary artery ligation model, oral gavage with 20 mg · kg-1 · day-1 simvastatin for 3 wk decreased (P < 0.05) mean arterial pressure (121 ± 20 vs. 96.5 ± 10.8 mmHg) and left ventricular change in pressure with time (4,500 ± 700 vs. 4,091 ± 1,064 mmHg/s, n = 6). Simvastatin reduced (P < 0.05) basal vasoconstriction and improved ACh-mediated vasorelaxation in CHF arterial rings. Inhibition of NO generation by NG-nitro-L-arginine methyl ester (100 µM) abolished the ACh-induced vasorelaxation in all rats. In conclusion, chronic treatment of CHF with simvastatin restores endothelial NO-dependent dysfunction and upregulates eNOS protein content in arterial tissue.

congestive heart failure; arterial relaxation; endothelial nitric oxide synthase; 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors


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