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
