The Function of Opioid Peptides Derived from Adrenal Medulla - Relationship to Stress and Immune System -

Methionine-enkephakin（Met-Enk）已知将与儿茶素（CA）进行共释放的肾上腺素细胞，当通过尼古丁乙酰胆碱素（Ach）受体刺激时。从肾上腺素gland释放的Met-Enk的生理作用是多少，至今还没有澄清。在这项研究中，发现了长时间暴露的bovine肾上腺素细胞（10微米）（6 - 24小时）导致了Met-Enk的连续释放，也是CA释放的一个瞬态。一种新识别的可移植性内分泌物，一种pituitary adenylate cyclase-激活多肽（PACAP，10 nM）提出了一种长期的CA和Met-Enk的秘密。CA在chromaffin细胞中的含量在长期治疗后没有被清除，但甚至被PACAP增加。PACAP-诱导的CA释放要求外部Ca-D12 + Ca-D1但未被电压操作的Ca-D12 + Ca-D1通道阻断器，A-激酶抑制剂，或C-激酶抑制剂。各种阿片类药物对CA r的影响 ... More 氯马芬细胞中的疾病也被调查过。Though Met-Enk是一个μ-，而δ-不支持这些子类型的CA版本。在对比度下， κ-抗酮就像Dynorphin A（1-13），明显减少了Ach-inducuced CA版本。这一抑制不是由k-特定的非特定的阿片类拮抗剂来拮抗的。（1-13） also inhibited Ach-induced intracellular Ca D12+ i D1 concentration rise in chromaffin cells。两种肾上腺素模拟， A（1-8）和A（2-13），发现在κ受体上没有或没有活动，显示出对A（1-13）的类似影响。在对比度高的KI-D1 + KI-D1-非PACAP-诱导的CA发布没有受到阿片类的影响。这些结果建议CA从肾上腺素细胞中释放的肾上腺素细胞不能被Met-Enk自动调节，但可以由另一个系统中的肾上腺素调节，因此κ类阿片从μ或δ类亚型中发挥不同的作用。Ach导致CA的瞬态释放，当PACAP被允许对CA成功的长期释放做出响应时，当PACAP被允许对成功的长期释放和Met-Enk生产进行响应时。Met-Enk的作用需要更远的调查。Less（低）

Methionine -enkephakin(Met-Enk) has been known to be co-released with catecholamine(CA) from adrenal medullary chromaffin cells when stimulated via nicotinic acetylcholine(Ach) receptor. The physiological role of released Met-Enk from adrenal gland, however, has not been clarified yet.In this study, it was found that a long time exposure (6 to 24 hrs) of bovine adrenal medullary chromaffin cells to nicotine (10μM) induced a continuous release of Met-Enk, although CA release was transient. A newly-identified putative endogenous secretagogue, pituitary adenylate cyclase-activating polypeptide (PACAP, 10nM) evoked a long-lasting secretion of CA and Met-Enk. The CA content in chromaffin cells was not decreased after long-term Ach treatment, but even increased by PACAP. PACAP-induced CA release required extracellular CaィイD12+ィエD1 but was not inhibited by voltage-operated CaィイD12+ィエD1 channel blockers, A-kinase inhibitors, nor C-kinase inhibitor.The effects of various opioid agonists on CA r … More elease in chromaffin cells were also investigated. Though Met-Enk is a μ-, and δ-agonists of these subtypes did not affect CA release. In contrast, κ-agonists like Dynorphin A(1-13) significantly reduced Ach-induced CA release. This inhibition was not antagonized by neither κ-specific nor non-specific opioid antagonists. Dynorphin A(1-13) also inhibited Ach-induced intracellular CaィイD12+ィエD1 concentration rise in chromaffin cells. Both dynorphin analogs, A(1-8) and A(2-13), which have been found to have less or no activity on κ-receptor, showed similar effects to A(1-13). In contrast, high KィイD1+ィエD1- nor PACAP-induced CA release was not affected by opioids. These results suggests that CA release from adrenal chromaffin cells is not autoregulated with Met-Enk, but may be regulated by another system involving dynorphin, thus κ subtype of opioids are plays different roles from μ or δ subtypes. Ach makes transient release of CA, while PACAP are supposed to be responsible for successive long-lasting release of CA, while PACAP are supposed to be responsible for successive long-lasting release and enhancement of Met-Enk production. The role of Met-Enk needs farther investigation. Less