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[Simvastatin attenuates cardiovascular effects and oxidative stress induced by angiotensin II]
S Delbosc1, J P Cristol, A Mimran
1Laboratoire de nutrition humaine et athérogenèse, Institut universitaire de recherche clinique, 641, av. Doyen-G.-Giraud, 34 295 Montpellier.
Abstract:
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.
Insights
Simvastatin, an HMG-CoA reductase inhibitor, reduced hypertension and cardiac hypertrophy in rats. This statin also partially prevented oxidative stress induced by angiotensin II, suggesting cardiovascular protective effects.
Area of Science:
- Pharmacology
- Cardiovascular Research
- Biochemistry
Context:
- Chronic angiotensin II (ANG II) infusion in rats induces hypertension, cardiac hypertrophy, and oxidative stress.
- HMG-CoA reductase inhibitors (statins) are widely used for cholesterol management.
- The role of statins in mitigating ANG II-induced cardiovascular damage requires further elucidation.
Purpose:
- To investigate the effects of simvastatin on the development of hypertension, cardiac hypertrophy, and oxidative stress induced by chronic ANG II administration in rats.
- To determine if simvastatin can attenuate the cardiovascular and oxidative consequences of sustained ANG II exposure.
Summary:
- Simvastatin (60 mg/Kg/24 h) was administered to rats 24 hours before and during 10 days of subcutaneous ANG II infusion (200 ng/Kg/min).
- Simvastatin significantly attenuated the development of hypertension (131 ± 9 vs 164 ± 4 mmHg) and cardiac mass increase (3.13 ± 0.09 vs 3.46 ± 0.09 mg/g).
- Simvastatin partially prevented the ANG II-induced overproduction of thiobarbituric acid reactive substances (TBARS), an indicator of lipid peroxidation (598 ± 40 vs 794 ± 79 pmol/mL).
Impact:
- Simvastatin demonstrates protective effects against angiotensin II-induced hypertension and cardiac hypertrophy in a rat model.
- The study suggests that simvastatin can mitigate oxidative stress, specifically lipid peroxidation, associated with chronic ANG II administration.
- These findings highlight the potential of statins in managing cardiovascular complications linked to the renin-angiotensin system.