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首页> 外文期刊>American Journal of Physiology >PPAR-gamma agonist rosiglitazone reverses increased cerebral venous hydraulic conductivity during hypertension.
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PPAR-gamma agonist rosiglitazone reverses increased cerebral venous hydraulic conductivity during hypertension.

机译：PPAR-γ激动剂罗格列酮可逆转高血压期间脑静脉液压传导性的增加。

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Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) agonists have been shown to protect the cerebral vasculature, including the blood-brain barrier. In the present study, we investigated the effect of the PPAR-gamma agonist rosiglitazone on changes in venous permeability during chronic hypertension induced by nitric oxide synthase inhibition. Female Sprague-Dawley rats were either treated with N(G)-nitro-L-arginine methyl ester (L-NAME; 0.5 g/l in drinking water) for 5 wk (HTN; n = 8), L-NAME for 5 wk plus the PPAR-gamma agonist rosiglitazone (20 mg/kg in food) for the last 3 wk (HTN + Rosi; n = 5), L-NAME for 5 wk plus the superoxide dismutase mimetic Tempol (1 mmol/l in drinking water) for the last 3 wk (HTN + Tempol; n = 8), or were untreated controls (n = 9). Fluid filtration (J(v)/S) and hydraulic conductivity (L(p)) of cerebral veins were compared in vitro between groups after a step increase in pressure from 10 to 25 mmHg to mimic the change in hydrostatic pressure during acute hypertension. Hypertension increased J(v)/S by 2.2-fold and L(p) by 3.2-fold. Rosiglitazone treatment after 2 wk of hypertension completely reversed the increased J(v)/S and L(p) that occurred during hypertension, whereas Tempol had no effect. These results demonstrate that rosiglitazone was effective at reversing changes in venous permeability that occurred during chronic hypertension, an effect that does not appear to be related to its antioxidant properties. Our findings suggest that PPAR-gamma may be a key regulator of blood-brain barrier permeability and a potential therapeutic target during hypertension.
机译：过氧化物酶体增殖物激活的受体-γ（PPAR-γ）激动剂已被证明可以保护脑血管系统，包括血脑屏障。在本研究中，我们研究了PPAR-γ激动剂罗格列酮对一氧化氮合酶抑制诱导的慢性高血压过程中静脉通透性变化的影响。将雌性Sprague-Dawley大鼠用N（G）-硝基-L-精氨酸甲酯（L-NAME;饮用水中0.5 g / l）处理5周（HTN; n = 8），L-NAME处理5周第3周（HTN + Rosi; n = 5），加上PPAR-γ激动剂罗格列酮（食品中20 mg / kg），第5周的L-NAME加超氧化物歧化酶模拟物Tempol（饮用时1 mmol / l）最后3周（HTN + Tempol; n = 8），或者是未经处理的对照组（n = 9）。在将压力从10 mmHg逐步增加到25 mmHg以模拟急性高血压期间静水压力的变化后，在两组之间进行了体外比较组之间脑静脉液过滤（J（v）/ S）和液压传导率（L（p））。高血压使J（v）/ S增加2.2倍，L（p）增加3.2倍。高血压2周后接受罗格列酮治疗可完全逆转高血压期间发生的J（v）/ S和L（p）升高，而Tempol无作用。这些结果表明，罗格列酮可有效逆转慢性高血压期间发生的静脉通透性变化，这种作用似乎与其抗氧化特性无关。我们的发现表明，PPAR-γ可能是血脑屏障通透性的关键调节剂，并且可能是高血压期间的潜在治疗靶标。

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