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首页> 外文期刊>Cellular Signalling >Modulation by propranolol of the uptake of ethidium bromide by rat submandibular acinar cells exposed to a P2X(7) agonist or to maitotoxin
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Modulation by propranolol of the uptake of ethidium bromide by rat submandibular acinar cells exposed to a P2X(7) agonist or to maitotoxin

机译：普萘洛尔对暴露于P2X（7）激动剂或人毒素的大鼠下颌腺腺泡细胞摄取溴化乙锭的调节作用

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We have compared the formation of pores in rat submandibular acinar cells in response to 2 ' ,3 ' -O-(4-benzoylbenzoyl) adenosine 5 ' -triphosphate (Bz-ATP) and maitotoxin. Bz-ATP (100 muM) permeabilized the cells to ethidium bromide. The uptake of ethidium increased to 29 +/- 1% of maximal uptake in 10 min. DL-Propranolol (300 muM) inhibited the Bz-ATP-induced uptake of ethidium bromide by 40% without affecting the P2X(7)-gated cation channel. The inhibitory effect of DL-propranolol on the formation of ports by Bz-ATP was reproduced by D-propranolol. an optical isomer with very poor beta -blocking activity. Tenidap. an antiinflammatory drug, enhanced the permeabilization in response to Bz-ATP. Propanolol inhibited the response to tenidap plus Bz-ATP. The effect of propranolol was reproduced by labetolol, a beta -adrenergic antagonist with membrane-stabilizing properties. but not by atenolol, which blocks beta -adrenergic receptors but has no effect on the stability of the membrane. In the presence of extracellular calcium, maitotoxin also increased the uptake of ethidium bromide. Tenidap had no effect on this response. which was delayed by propranolol. In conclusion, we have shown that propranolol. in a range of 10-300 muM, inhibits the pore-forming activity of the P2X(7) receptor without affecting the opening of the cation channel coupled to this receptor. This inhibition is not related to its beta -adrenergic blocking activity bur rather to its membrane-stabilizing: properties. Propranolol also delays the uptake of ethidium bromide in response to maitotoxin. This is in agreement with the current view that P2X(7) agonists and maitotoxin share a common pore. (C) 2001 Elsevier Science Inc. All rights reserved. [References: 42]
机译：我们已经比较了响应2'，3'-O-（4-苯甲酰基苯甲酰基）腺苷5'-三磷酸（Bz-ATP）和毛毒素的大鼠下颌腺泡细胞中孔的形成。 Bz-ATP（100μM）使细胞通透溴化乙锭。在10分钟内，乙锭的摄取增加到最大摄取的29 +/- 1％。 DL-普萘洛尔（300μM）在不影响P2X（7）门控的阳离子通道的情况下将Bz-ATP诱导的溴化乙锭的摄取抑制了40％。 DL-普萘洛尔再现了DL-普萘洛尔对Bz-ATP形成的端口的抑制作用。一种β阻滞活性非常差的旋光异构体。 Tenidap。一种抗炎药，可增强对Bz-ATP的通透性。普萘洛尔抑制对tenidap加Bz-ATP的反应。拉贝洛尔是一种具有膜稳定特性的β-肾上腺素能拮抗剂，可复制普萘洛尔的作用。但不是阿替洛尔，它可以阻断β-肾上腺素受体，但对膜的稳定性没有影响。在细胞外钙的存在下，麦芽毒素也增加了溴化乙锭的摄取。 Tenidap对此反应没有影响。普萘洛尔延误了治疗。总之，我们已经证明了普萘洛尔。在10-300μM的范围内，抑制P2X（7）受体的成孔活性，而不会影响与该受体偶联的阳离子通道的打开。这种抑制作用与其β-肾上腺素阻断活性bur不相关，而与其膜稳定性质有关。普萘洛尔还响应于人毒素而延迟溴化乙锭的摄取。这与当前的观点一致，即P2X（7）激动剂和麦托毒素具有共同的孔。 （C）2001 Elsevier Science Inc.保留所有权利。 [参考：42]

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