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A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats
Published on: December 2, 2016
Beneficial effects of rosuvastatin on aortic adverse remodeling in nitric oxide-deficient rats
Rodrigo Neto-Ferreira1, Vinícius Novaes Rocha, Thiago da Silva Torres
1Laboratory of Ultrastructure and Tecidual Biology, Biomedical Center, Institute of Biology, State University of Rio de Janeiro, Brazil. rnvetferreira@hotmail.com
Abstract:
This study aimed to evaluate the effect of rosuvastatin upon structural and ultrastructural aortic remodeling in a rat model of hypertension induced by NO synthase blockade. Wistar rats were divided into 4 groups: Control group (C); control treated with rosuvastatin 20mg/kg/day (CR); L-NAME group 40 mg/kg/day (LN) and L-NAME treated with rosuvastatin (LNR) (same doses). Body mass and blood pressure were measured weekly; the experiment lasted 5 weeks. L-NAME administration augmented blood pressure (BP) in the LN group in comparison to the C group (123.3 vs. 180.5 mm Hg at week 5). In LNR rats, rosuvastatin slightly attenuated BP rise, but it had no effect on the BP of CR group. Intima and media thickening of the thoracic aorta were observed in the LN group, and increased elastic fiber content as well. Rosuvastatin prevented all these alterations as seen in the LNR group. Ultrastructural changes due to L-NAME intake (intracellular vesicles and altered membrane morphology in endothelial cells, extracellular matrix deposition, and cytoplasmatic projections from smooth muscle cells toward the internal elastic lamina) were also prevented by rosuvastatin. All in all, rosuvastatin administration is capable of attenuating ultrastructural aortic wall remodeling in NO-deficient rats despite small changes in blood pressure.
Insights
Rosuvastatin treatment prevented aortic wall remodeling in rats with hypertension caused by nitric oxide synthase blockade. This study shows rosuvastatin
Area of Science:
- Cardiovascular Biology
- Pharmacology
- Hypertension Research
Background:
- Hypertension is linked to significant aortic structural and ultrastructural changes.
- Nitric oxide synthase (NOS) blockade is a model for inducing hypertension and studying its vascular effects.
- Statins, like rosuvastatin, are known for lipid-lowering and potential pleiotropic effects.
Purpose of the Study:
- To investigate the impact of rosuvastatin on aortic remodeling in a rat model of hypertension induced by NOS blockade.
- To assess rosuvastatin's effects on both structural and ultrastructural alterations in the aorta.
- To determine if rosuvastatin can mitigate hypertension-induced vascular damage.
Main Methods:
- Wistar rats were divided into four groups: Control (C), Control + Rosuvastatin (CR), L-NAME (hypertension model), and L-NAME + Rosuvastatin (LNR).
- Rosuvastatin (20mg/kg/day) and L-NAME (40mg/kg/day) were administered for 5 weeks.
- Blood pressure and body mass were monitored weekly. Thoracic aorta sections were analyzed for structural and ultrastructural changes.
Main Results:
- L-NAME induced significant hypertension (180.5 vs 123.3 mm Hg).
- Rosuvastatin slightly attenuated the blood pressure rise in LNR rats but did not affect normotensive rats.
- L-NAME caused intima-media thickening, increased elastic fibers, and endothelial/smooth muscle cell ultrastructural changes, all of which were prevented by rosuvastatin in the LNR group.
Conclusions:
- Rosuvastatin effectively prevented structural and ultrastructural aortic wall remodeling in rats with L-NAME-induced hypertension.
- These protective effects occurred despite only a slight attenuation of blood pressure elevation.
- The findings suggest rosuvastatin has beneficial vascular protective properties independent of significant BP reduction in this model.
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