Regulation of catecholamine release in human adrenal chromaffin cells by β-adrenoceptors
Regulation of catecholamine release in human adrenal chromaffin cells by β-adrenoceptors
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DOI：
10.1016/j.neuint.2011.12.018
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发表时间：
2012-03-01
影响因子：
4.2
通讯作者：
Cavadas, Claudia
中科院分区：
文献类型：
--
作者：
Cortez, Vera;Santana, Magda;Cavadas, Claudia
肾上腺在对各种压力情况的反应中起着重要作用。应激状态后，肾上腺髓质嗜铬细胞通过胞吐释放大量儿茶酚胺（肾上腺素，EP;去甲肾上腺素，NE），尤其是EP。一旦进入血流，儿茶酚胺到达不同的靶器官，并通过激活不同的肾上腺素受体诱导其生物学作用。肾上腺细胞也可以通过激素、旁分泌和/或自分泌系统被儿茶酚胺激活。以前没有评估人肾上腺髓质上功能性肾上腺素受体的存在及其对儿茶酚胺分泌的参与。本研究观察了β（1）、β（2）和β（3）肾上腺素能受体激动剂异丙肾上腺素（isoproterenol）和β（2）肾上腺素能受体激动剂沙丁胺醇（salbuttamine）刺激人肾上腺嗜铬细胞释放儿茶酚胺（NE和EP）的作用。此外，β（2）-肾上腺素能受体拮抗剂（ICI 118，551; 100 nM）和β（3）-肾上腺素能受体拮抗剂（SR 59230 A; 100 nM）可抑制嗜铬细胞中异丙肾上腺素和尼古丁刺激的儿茶酚胺释放。β（1）-肾上腺素受体拮抗剂（阿替洛尔; 100 nM）不改变异丙肾上腺素-也不改变尼古丁诱发的人肾上腺嗜铬细胞释放的儿茶酚胺。此外，我们的研究结果表明，蛋白激酶A（PKA），蛋白激酶C（PKC），丝裂原活化蛋白激酶（MAPK）和磷脂酶C（PLC）参与的细胞内机制引起的沙丁胺醇的释放。总之，我们的数据表明，β（2）-和β（3）-肾上腺素受体的激活调节基础和诱发的儿茶酚胺释放，NE和EP，通过自分泌正反馈回路在人肾上腺嗜铬细胞。(C)2012爱思唯尔有限公司保留所有权利。
The adrenal gland plays a fundamental role in the response to a variety of stress situations. After a stress condition, adrenal medullary chromaffin cells release, by exocytosis, high quantities of catecholamine (epinephrine, EP; norepinephrine, NE), especially EP. Once in the blood stream, catecholamines reach different target organs, and induce their biological actions through the activation of different adrenoceptors. Adrenal gland cells may also be activated by catecholamines, through hormonal, paracrine and/or autocrine system. The presence of functional adrenoceptors on human adrenal medulla and their involvement on catecholamines secretion was not previously evaluated. In the present study we investigated the role of beta(1)-, beta(2)- and beta(3)-adrenoceptors on catecholamine release from human adrenal chromaffin cells in culture.We observed that the beta-adrenoceptor agonist (isoproterenol) and beta(2)-adrenoceptor agonist (salbutamol) stimulated catecholamine (NE and EP) release from human adrenal chromaffin cells. Furthermore, the beta(2)-adrenoceptor antagonist (ICI 118,551; 100 nM) and beta(3)-adrenoceptor antagonist (SR 59230A; 100 nM) inhibited the catecholamine release stimulated by isoproterenol and nicotine in chromaffin cells. The beta(1)-adrenoceptor antagonist (atenolol; 100 nM) did not change the isoproterenol- neither the nicotine-evoked catecholamine release from human adrenal chromaffin cells. Moreover, our results show that the protein kinase A (PKA), protein kinase C (PKC), mitogen-activated protein kinase (MAPK) and phospholipase C (PLC) are intracellular mechanisms involved in the catecholamine release evoked by salbutamol. In conclusion, our data suggest that the activation of beta(2)- and beta(3)-adrenoceptors modulate the basal and evoked catecholamine release, NE and EP, via an autocrine positive feedback loop in human adrenal chromaffin cells. (C) 2012 Elsevier Ltd. All rights reserved.