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首页> 外文期刊>The Korean Journal of Physiology & Pharmacology >Resveratrol Inhibits Nicotinic Stimulation-Evoked Catecholamine Release from the Adrenal Medulla
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Resveratrol Inhibits Nicotinic Stimulation-Evoked Catecholamine Release from the Adrenal Medulla

机译：白藜芦醇抑制从肾上腺髓质中释放出烟熏刺激引起的儿茶酚胺。

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Resveratrol has been known to possess various potent cardiovascular effects in animal, but there is little information on its functional effect on the secretion of catecholamines (CA) from the perfused model of the adrenal medulla. Therefore, the aim of the present study was to determine the effect of resveratrol on the CA secretion from the isolated perfused model of the normotensive rat adrenal gland, and to elucidate its mechanism of action. Resveratrol (10~100μM) during perfusion into an adrenal vein for 90 min inhibited the CA secretory responses evoked by ACh (5.32 mM), high K+ (a direct membrane-depolarizer, 56 mM), DMPP (a selective neuronal nicotinic Nn receptor agonist, 100μM) and McN-A-343 (a selective muscarinic M1 receptor agonist, 100μM) in both a time- and dose-dependent fashion. Also, in the presence of resveratrol (30μM), the secretory responses of CA evoked by veratridine 8644 (an activator of voltage-dependent Na+ channels, 100μM), Bay-K-8644 (a L-type dihydropyridine Ca2+ channel activator, 10μM), and cyclopiazonic acid (a cytoplasmic Ca2+-ATPase inhibitor, 10μM) were significantly reduced. In the simultaneous presence of resveratrol (30μM) and L-NAME (an inhibitor of NO synthase, 30μM), the CA secretory evoked by ACh, high K+ , DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid were recovered to a considerable extent of the corresponding control secretion compared with the inhibitory effect of resveratrol alone. Interestingly, the amount of nitric oxide (NO) released from the adrenal medulla was greatly increased in comparison to its basal release. Taken together, these experimental results demonstrate that resveratrol can inhibit the CA secretory responses evoked by stimulation of cholinergic nicotinic receptors, as well as by direct membrane-depolarization in the isolated perfused model of the rat adrenal gland. It seems that this inhibitory effect of resveratrol is exerted by inhibiting an influx of both ions through Na+ and Ca2+ channels into the adrenomedullary cells as well as by blocking the release of Ca2+ from the cytoplasmic calcium store, which are mediated at least partly by the increased NO production due to the activation of NO synthase.
机译：已知白藜芦醇在动物中具有多种有效的心血管作用，但是从肾上腺髓质的灌注模型中关于其对儿茶酚胺（CA）分泌的功能作用的信息很少。因此，本研究的目的是确定白藜芦醇对正常血压大鼠肾上腺灌注模型的CA分泌的影响，并阐明其作用机理。白藜芦醇（10〜100μM）灌注至肾上腺静脉90分钟可抑制ACh（5.32 mM），高K + （直接膜去极化剂56 mM），DMPP引起的CA分泌反应（选择性神经元烟碱N n 受体激动剂100μM）和McN-A-343（选择性毒蕈碱M 1 受体激动剂100μM）的时间和剂量依赖的时尚。此外，在白藜芦醇（30μM）存在的情况下，维拉替啶8644（电压依赖性Na + 通道的激活剂，100μM），Bay-K-8644（一种L-二氢吡啶类Ca 2 + 通道激活剂（10μM）和环吡嗪酸（胞质Ca 2 + -ATPase抑制剂10μM）显着降低。在同时存在白藜芦醇（30μM）和L-NAME（NO合酶抑制剂30μM）的情况下，ACh，高K + ，DMPP，McN-A-343，Bay引起的CA分泌与单独的白藜芦醇的抑制作用相比，回收到-K-8644和环吡嗪酸的程度相当大，具有相应的对照分泌物。有趣的是，与基础释放相比，从肾上腺髓质释放的一氧化氮（NO）的量大大增加了。综上所述，这些实验结果表明白藜芦醇可以抑制胆碱能烟碱样受体的刺激以及在大鼠肾上腺的灌注模型中通过直接的膜去极化引起的CA分泌反应。白藜芦醇的这种抑制作用似乎是通过抑制两个离子通过Na + 和Ca 2 + 通道流入肾上腺髓质细胞并阻止其释放而发挥的。胞质钙库中Ca 2 + 的表达至少部分是由于NO合酶的活化导致NO生成增加所介导的。

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