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首页> 外文期刊>American Journal of Physiology >Purinergic receptors contribute to early mesangial cell transformation and renal vessel hypertrophy during angiotensin II-induced hypertension
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Purinergic receptors contribute to early mesangial cell transformation and renal vessel hypertrophy during angiotensin II-induced hypertension

机译：嘌呤能受体有助于血管紧张素II诱发的高血压期间早期系膜细胞转化和肾血管肥大

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First published November 7, 2007; doi:10.1152/ajprenal.00281.2007.-Chronic ANG II infusions lead to increases in intrarenal ANG II levels, hypertension, and tissue injury. Increased blood pressure also elicits increases in renal interstitial fluid (RIF) ATP concentrations that stimulate cell proliferation. We evaluated the contribution of purinergic receptor activation to ANG II-induced renal injury in rats by treating with clopidogrel, a P2Y12 receptor blocker, or with PPADS, a nonselective P2 receptor blocker. a-Actin expression in mesangial cells, afferent arteriolar wall thickness (AAWT), cortical cell proliferation, and macrophage infiltration were used as early markers of renal injury. Clopidogrel and PPADS did not alter blood pressure, renin or kidney ANG II content. a-Actin expression increased from control of 0.6 +- 0.4% of mesangial area to 6.3 +- 1.9% in ANG D-infused rats and this response was prevented by clopidogrel (0.4 +- 0.2%) and PPADS. The increase in AAWT from 4.7 +- 0.1 to 6.0 +- 0.1 mm in ANG E rats was also prevented by clopidogrel (4.8 +- 0.1 mm) and PPADS. ANG II infusion led to interstitial macrophage infiltration (105 +- 16 vs. 62 +-4 cell/mm2) and tubular proliferation (71 +- 15 vs. 20 +- 4 cell/mm2) and these effects were prevented by clopidogrel (52 +- 4 and 36 +- 3 cell/mm2) and PPADS. RIF ATP levels were higher in ANG II-infusedrats than in control rats (11.8 +- 1.9 vs. 5.6 +- 0.6 nmoJ/1, P < 0.05). The results suggest that activation of vascular and glomerular purinergic P2 receptors may contribute to the mesangial cell transformation, renal inflammation, and vascular hypertrophy observed in ANG Il-dependent hypertension.
机译：首次发布于2007年11月7日; doi：10.1152 / ajprenal.00281.2007.-长期ANG II输注会导致肾内ANG II水平升高，高血压和组织损伤。血压升高还会引起肾间质液（RIF）ATP浓度升高，从而刺激细胞增殖。我们通过用P2Y12受体阻断剂氯吡格雷或非选择性P2受体阻断剂PPADS治疗，评估嘌呤能受体激活对ANG II诱导的大鼠肾损伤的作用。肾小球系膜细胞中α-肌动蛋白的表达，传入小动脉壁厚度（AAWT），皮质细胞增殖和巨噬细胞浸润被用作肾损伤的早期标志物。氯吡格雷和PPADS不会改变血压，肾素或肾脏ANG II含量。在注入ANG D的大鼠中，α-肌动蛋白的表达从控制的肾小球膜面积的0.6±0.4％增加到6.3±1.9％，氯吡格雷（0.4±0.2％）和PPADS阻止了这种反应。氯吡格雷（4.8±0.1 mm）和PPADS也可以防止ANG E大鼠的AAWT从4.7±0.1 mm增加到6.0±0.1 mm。 ANG II输注导致间质巨噬细胞浸润（105 +-16 vs. 62 + -4细胞/ mm2）和肾小管增生（71 +-15 vs. 20 + -4细胞/ mm2），而氯吡格雷预防了这些作用（52 +-4和36 +-3 cell / mm2）和PPADS。输注ANG II的大鼠的RIF ATP水平高于对照组大鼠（11.8±1.9 vs. 5.6±0.6 nmoJ / 1，P <0.05）。结果表明血管和肾小球嘌呤能P2受体的激活可能有助于血管紧张素II依赖性高血压中观察到的肾小球膜细胞转化，肾炎和血管肥大。

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