Key result
Early nitrendipine delays hypertension development and reverses mesenteric artery remodeling in hypertensive rats.
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In this study we evaluated the delayed effects of a calcium entry blocker on blood pressure and on vascular structural and functional alterations in mesenteric resistance arteries of spontaneously hypertensive rats (SHR). The calcium entry blocker nitrendipine was administered (30 mg/kg per day) according to three different schedules: in one group of SHR from 4 to 8 weeks of age (n = 12), in a second group from 8 to 12 weeks of age (n = 12), and in a third group from 4 to 12 weeks of age (n = 12). Twelve untreated SHR and 12 untreated Wistar-Kyoto rats served as controls. Half the animals of each group were killed at 13 weeks, and the remaining were killed at 38 weeks. After death, relative left ventricular mass was calculated. Vascular morphology and function (responses to norepinephrine and acetylcholine) in mesenteric small arteries were then assessed using a micromyographic technique. Nitrendipine treatment delayed the development of hypertension and determined the regression of structural alterations of mesenteric resistance arteries in SHR. These favorable effects were maintained for several weeks after treatment withdrawal, provided that treatment was started at 4 weeks of age. Considering the functional alterations of mesenteric arteries in SHR (responses to norepinephrine and acetylcholine), nitrendipine treatment determined an improvement of both these dysfunctions as long as reductions of the media-to-lumen ratio and blood pressure, respectively, were maintained.
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Rizzoni et al. (1994) studied Hypertension (spontaneously hypertensive rats) (n=60). Nitrendipine vs. Untreated spontaneously hypertensive rats and untreated Wistar-Kyoto rats was evaluated on Blood pressure, relative left ventricular mass, and vascular structural and functional alterations in mesenteric resistance arteries. Nitrendipine started at 4 weeks of age delayed hypertension and regressed mesenteric artery structural and functional alterations in SHR after withdrawal.
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