Abstract
This study investigated the beneficial effects of D-α-tocopherol supplementation in protecting against the renal morphological and functional changes caused by hypertension. Spontaneously hypertensive (SHR) and normotensive control (WKY) rats received D-α-tocopherol (80 mg/kg by gavage) or vehicle (mineral oil) every other day for 60 days, from the age of 2 months. After this treatment period, all animals were assessed for renal morphological and functional parameters. The glomerular hypertrophy, increased interlobular wall thickness and enlarged renal vascular resistance found in SHR were reduced by D-α-tocopherol treatment. Sodium and volume retention observed in SHR were also decreased by D-α-tocopherol treatment. Moreover, D-α-tocopherol supplementation significantly reduced arterial pressure in SHR but not in WKY. D-α-tocopherol also reduced the excretion of thiobarbituric acid-reactive substances (TBARS), a marker of oxidative stress, in SHR. These results suggest that D-α-tocopherol supplementation can reduce kidney damage induced by hypertension.
Highlights
Besides representing a significant cardiovascular risk factor and major contributor to renal damage, hypertension alone is a serious public-health problem worldwide (Kearney et al, 2005)
Considering the effect of D-a-tocopherol on antioxidant enzymes, and that hypertension and increased exposure to Reactive oxygen species (ROS) can lead to renal dysfunction, the present study investigated whether D-a-tocopherol treatment can reduce the alterations of glomerular and renal vascular morphology observed in spontaneously hypertensive (SHR) and in renal function parameters
Body weight was higher in hypertensive rats than in normotensive controls (313 ± 9 vs. 277 ± 7 g)
Summary
Besides representing a significant cardiovascular risk factor and major contributor to renal damage, hypertension alone is a serious public-health problem worldwide (Kearney et al, 2005). Increased systemic blood pressure can be transmitted to the glomeruli leading to progressive renal injury which, in turn, can aggravate systemic hypertension (Fogo, 2000; Marcantoni et al, 2000). Over the last two decades, oxidative stress has been shown to play an important role in the pathogenesis of hypertension. Reactive oxygen species (ROS) are thought to act through several mechanisms to mediate vascular changes. ROS can directly affect endothelial and vascular smooth muscle cells, resulting in structural and functional damage, can scavenge or inactivate endothelium relaxing factors such as NO and prostacyclin and may stimulate the production of peroxynitrite, a potent constrictor. ROS imbalance is associated to glomerular and tubular dysfunction as well as sodium retention (Nistala et al, 2008)
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