Journal
NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY
Volume 385, Issue 12, Pages 1199-1209Publisher
SPRINGER
DOI: 10.1007/s00210-012-0798-z
Keywords
Two-kidney; one-clip hypertension; Euterpe oleracea Mart; Endothelial dysfunction; Oxidative stress; Vascular remodeling
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Funding
- National Council of Scientific and Technological Development (CNPq)
- Rio de Janeiro State Research Agency (FAPERJ)
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The consumption of polyphenol-rich foods is associated with a decreased risk of mortality from cardiovascular diseases. Previously, we have demonstrated that the stone of Euterpe oleracea Mart. (a double dagger ai) from the Amazon region exerts vasodilator and antioxidant actions. This study examined the effect of a double dagger ai stone extract (ASE) on the vascular functional and structural changes and oxidative stress associated with the two-kidney, one-clip (2K-1C) renovascular hypertension. 2K-1C and sham-operated rats were treated with ASE 200 mg/kg/day (or vehicle) for 40 days. Blood pressure was measured by tail plethysmography, and the vascular reactivity was evaluated in the rat isolated mesenteric arterial bed. Mesenteric protein expression of endothelial nitric oxide synthase (eNOS), superoxide dismutase 1 and 2 (SOD1 and SOD2), metalloproteinase 2 (MMP-2), and tissue inhibitor of MMPs (TIMP)-1 was assessed by Western blot; oxidative damage and antioxidant activity by spectrophotometry; MMP-2 levels by gelatin zymography; and structural changes by histological analysis. ASE prevented 2K-1C hypertension and the reduction of acetylcholine-induced vasodilation. The increased levels of malondialdehyde and carbonyl protein were reduced by ASE. SOD, catalase, and glutathione peroxidase activities and the expressions of SOD1 and SOD2, eNOS, and TIMP-1 were decreased in 2K-1C rats and recovered by ASE. In 2K-1C rats, ASE prevented vascular remodeling and the increased expression/levels of MMP-2. These findings indicate that ASE produces antihypertensive effect and prevents the endothelial dysfunction and vascular structural changes in 2K-1C hypertension, probably through mechanisms involving antioxidant effects, NOS activation, and inhibition of MMP-2 activation.
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