Abstract
Ellagic acid is described as having antioxidant and antiproliferative properties. Hence, it was hypothesized that ellagic acid could improve cardiovascular damage caused by hypertension. In this work, hypertension was induced in rats with Nω-Nitro-L-arginine methyl ester hydrochloride (60 mg/kg/day in drinking water) for 6 weeks. Ellagic acid was coadministered (10 or 30 mg/kg/day by gavage) between the second and sixth week. Blood pressure was recorded every week by tail-cuff plethysmography. After 6 weeks, the rats were sacrificed, the hearts and kidneys were weighed, and blood was collected. Aortas were isolated and set up to isometric recordings in an organ bath for histological assay and measuring of calcium content. Hypertension (233.6 ± 9.5 mmHg) was reduced (p < 0.01) by treatment with ellagic acid 10 or 30 mg/kg. The blood levels of nitrate/nitrite were reduced in hypertensive rats and the ellagic acid restored these levels. While the vascular relaxations to acetylcholine and sodium nitoprusside and the contraction to phenylephrine were impaired in the hypertensive group, they were improved after ellagic acid treatment. The alkaline phosphatase activity was increased by hypertension and returned to control levels after ellagic acid treatment. In the aorta, the administration of ellagic acid resulted in less aortic wall thickening and less calcification. In conclusion, ellagic acid attenuates hypertension, possibly improving nitric oxide bioavailability. The vascular response to acetylcholine, sodium nitroprusside, and phenylephrine was impaired by hypertension and improved after treatment with ellagic acid. Moreover, plasmatic alkaline phosphatase activity, calcium content, and hypertrophy in vascular tissues during hypertension were attenuated by treatment with ellagic acid.
Key words
ellagic acid - alkaline phosphatase - aortas - vascular relaxation - hypertension
