Ca(2+)-dependent stimulatory effect of pituitary adenylate cyclase-activating polypeptide on catecholamine secretion from cultured porcine adrenal medullary chromaffin cells.
Ca(2+)-dependent stimulatory effect of pituitary adenylate cyclase-activating polypeptide on catecholamine secretion from cultured porcine adrenal medullary chromaffin cells.
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垂体腺苷酸环化酶激活多肽对培养猪肾上腺髓质嗜铬细胞儿茶酚胺分泌的 Ca(2) 依赖性刺激作用。
DOI：
10.1210/endo.132.4.8384995
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发表时间：
1993
期刊：
影响因子：
4.8
通讯作者：
Yoh Takuwa
中科院分区：
文献类型：
--
作者：
K. Isobe;T. Nakai;Yoh Takuwa
腺苷酸环化酶激活多肽（PACAP）以剂量依赖性方式刺激培养的猪肾上腺髓质嗜铬细胞分泌儿茶酚胺，半最大剂量和最大剂量分别为30 nM和1 μ M。去除细胞外Ca ~（2+）或加入无机Ca ~（2+）通道阻滞剂Gd ~（3+）均能有效抑制PACAP诱导的儿茶酚胺分泌。尼卡地平（1 μ M）和甲氧基维拉帕米（1 μ M），电压依赖性钙通道的阻断剂，也有效抑制PACAP诱导的儿茶酚胺分泌。当在Fura 2负载的单个嗜铬细胞中测量细胞内游离Ca 2+浓度（[Ca 2 +]i）时，发现PACAP通过从细胞外和细胞内池中动员Ca 2+而引起[Ca 2 +]i的持续增加。还发现PACAP以剂量依赖性方式刺激肌醇磷酸的产生，这不像尼古丁的情况那样通过去除细胞外Ca 2+而被消除。PACAP以剂量依赖性方式增加嗜铬细胞中的cAMP含量。去除细胞外Ca 2+增强PACAP诱导的cAMP产生，但强烈抑制PACAP诱导的儿茶酚胺分泌。用腺苷-3 '：5'-单硫代磷酸酯，环状，Rp-异构体，一种cAMP拮抗剂预处理细胞，不阻断PACAP诱导的儿茶酚胺分泌。此外，毛喉素或3-异丁基-1-甲基黄嘌呤不增强PACAP诱导的儿茶酚胺分泌。这些结果表明，PACAP激活培养的猪肾上腺髓质细胞的电压依赖性Ca ~（2+）通道和磷脂酶C以及腺苷酸环化酶，并强烈表明，PACAP诱导的儿茶酚胺分泌主要是通过激活电压依赖性Ca ~（2+）通道介导的。
Pituitary adenylate cyclase-activating polypeptide (PACAP) stimulates catecholamine secretion from cultured porcine adrenal medullary chromaffin cells in a dose-dependent manner with the half-maximal and maximal doses of 30 nM and 1 microM, respectively. Either removal of extracellular Ca2+ or addition of Gd3+, an inorganic Ca2+ channel blocker, very potently inhibits PACAP-induced catecholamine secretion. Both nicardipine (1 microM) and methoxyverapamil (1 microM), blockers of voltage-dependent Ca2+ channels, are also effective in inhibiting PACAP-induced catecholamine secretion. When the intracellular free Ca2+ concentration ([Ca2+]i) is measured in a fura 2-loaded single chromaffin cell, PACAP is found to cause a sustained increase in [Ca2+]i by mobilizing Ca2+ from both extra- and intracellular pools. It is also found that PACAP stimulates the production of inositol phosphates in a dose-dependent manner, which is not abolished by removal of extracellular Ca2+ unlike the case of nicotine. PACAP increases cAMP content in chromaffin cells in a dose-dependent manner. Removal of extracellular Ca2+ enhances PACAP-induced cAMP production but strongly inhibits PACAP-induced catecholamine secretion. Pretreatment of cells with adenosine-3':5'-monophosphothioate, cyclic, Rp-isomer, a cAMP antagonist, does not block PACAP-induced catecholamine secretion. The addition of forskolin or 3-isobutyl-1-methylxanthine does not enhance the PACAP-induced catecholamine secretion. These results indicate that PACAP activates voltage-dependent Ca2+ channels and phospholipase C as well as adenylate cyclase in cultured porcine adrenal medullary cells and strongly suggest that PACAP-induced catecholamine secretion is mainly mediated by activation of voltage-dependent Ca2+ channels.
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DOI：
10.1016/s0021-9258(18)33559-2
发表时间：
1982-11
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
J. Haycock;J. Meligeni;W. Bennett;J. Waymire
通讯作者：
J. Haycock;J. Meligeni;W. Bennett;J. Waymire
牛肾上腺嗜铬细胞的胞吐作用不需要激活蛋白激酶 C。
DOI：
--
发表时间：
1990
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Terbush,DR;Holz,RW
通讯作者：
Holz,RW
DOI：
10.1016/0006-291x(90)92140-u
发表时间：
1990-07-31
影响因子：
3.1
作者：
MIYATA, A;JIANG, L;ARIMURA, A
通讯作者：
ARIMURA, A
糖皮质激素和环AMP对酪氨酸羟化酶基因的转录调节。
DOI：
10.1073/pnas.84.11.3550
发表时间：
1987
影响因子：
11.1
作者：
Lewis,EJ;Harrington,CA;Chikaraishi,DM
通讯作者：
Chikaraishi,DM
垂体产生白细胞介素 6 的神经肽调节：垂体腺苷酸环化酶激活多肽和降钙素基因相关肽的刺激。
影响因子：
4.8
作者：
Tatsuno,I;Somogyvari-Vigh,A;Mizuno,K;Gottschall,PE;Hidaka,H;Arimura,A
通讯作者：
Arimura,A