Résumé
The effects of an HMG-CoA reductase inhibitor, simvastatin (statin, 60 mg/Kg/24 h by forced feeding), were studied on the development of hypertension, cardiac hypertrophy and oxidating stress induced by chronic perfusion of angiotensin II (ANG II, 200 ng/Kg/min s.c., for 10 days) in the rat. The statin was giver 24 hours before, and during the 10 days of ANG II. At the end of the study, mean blood pressure was measured and blood sampling performed under anaesthesia (sodium pentobarbital). The cardiac mass index was measured (cardiac mass/body weight, mg/Kg). TBARS (thiobarbituric acid reactive substances), representing the index of lipid peroxidation, was assessed by fluorimetry. The statin attenuated the development of hypertension (131 +/- 9 vs 164 +/- 4 mmHg) and the increase in cardiac mass (3.13 +/- 0.09 vs 3.46 +/- 0.09 mg/g) associated with ANG II. The overproduction of TBARS induced by ANG II was partially prevented by simvastatin (598 +/- 40 vs 794 +/- 79 pmol/mL). These results indicate that simvastatin attenuates the cardiovascular effects and lipid peroxidation induced by chronic administration of angiotensin II.The effects of an HMG-CoA reductase inhibitor, simvastatin (statin, 60 mg/Kg/24 h by forced feeding), were studied on the development of hypertension, cardiac hypertrophy and oxidating stress induced by chronic perfusion of angiotensin II (ANG II, 200 ng/Kg/min s.c., for 10 days) in the rat. The statin was giver 24 hours before, and during the 10 days of ANG II. At the end of the study, mean blood pressure was measured and blood sampling performed under anaesthesia (sodium pentobarbital). The cardiac mass index was measured (cardiac mass/body weight, mg/Kg). TBARS (thiobarbituric acid reactive substances), representing the index of lipid peroxidation, was assessed by fluorimetry. The statin attenuated the development of hypertension (131 +/- 9 vs 164 +/- 4 mmHg) and the increase in cardiac mass (3.13 +/- 0.09 vs 3.46 +/- 0.09 mg/g) associated with ANG II. The overproduction of TBARS induced by ANG II was partially prevented by simvastatin (598 +/- 40 vs 794 +/- 79 pmol/mL). These results indicate that simvastatin attenuates the cardiovascular effects and lipid peroxidation induced by chronic administration of angiotensin II.