Study of the secretion of atrial natriuretic peptide (ANP) induced by morphine.

吗啡诱导心房钠尿肽（ANP）分泌的研究。

基本信息

批准号：
63570717
负责人：
KUDO Tsuyoshi
金额：
$ 0.96万
依托单位：
Hirasaki University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1988
资助国家：
日本
起止时间：
1988 至 1989
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-63570717/
关键词：
ANP Morphine Enkepharin Dynorphin Catecholamine Rat Atrium cell Naloxane フェンタニールオピオイド受容体 c-GMP ACTH CompB

项目摘要

1)In vivo experiment: Effects of morphine, feritanyl, dynorphin, enkepharin, beta-endorphin and naloxone on immunoreactive atrial natriuretic peptide (ir-ANP) levels in the plasma were investigated in conscious and unstrained male wistar rats. High dose of morphine and fentanyl induced a significant increase in plasma levels of ir-ANP concentration, but none of other opioide peptides induced such a increase. Significant increases in plasma cyclic GMP levels as well as ir-ANP were observed in morphine and fentanyl groups. Cyclic GMP was strongly implicated as a second messenger for ir-ANP. The increase in plasma cyclic GMP was well correlated with the increase of plasma ir-ANP levels. These significant increases were completely blocked by naloxone which was a strong, antagonist to opiate receptor of mu type. These results suggest that a high dose of morphine would increase plasma ir-ANP via morphine receptor. Furthermore, the marked increases of plasma catecholamine (NE and E) were observed as well as ir-ANP and cGMP by morphine and fentanyl. This observation would indicate a possible involvement of endogeneous catecholamine with opiate receptor in the reguration of ir-ANP secretion.2)In vitro experiment: The rat atrium cells were obtained by the enzyme dissociation of atrium. The cells were incubated with opioide peptides and catecholamines under the condition of 95% O and 5% CO with 38 C for 4 h. The concentration of ir-ANP in medium of culture tubes were increased by dynorphin and catecholamine but not another peptide. The combination of dynorphin and catecholamine markedly increased ir-ANP secretion from atrium cells, Especially. the combination with dopamine induced 10 fold increase than that of NE and E. These increase in ir-ANP were not blocked by naloxone.These results from the experiments of in vivo and in vitro suggest that endogeneous catecholamines involved in the secretion of ANP induced by large dose of morphine.

1）体内实验：在有意识和未经训练的雄性Wistar Rats中研究了吗啡，Feritanyl，dynorphin，ankepharin，Enkepharin，beta-Endorphin和Naloxone对血浆中质量下的免疫反应性心房肽（IR-ANP）水平的影响。高剂量的吗啡和芬太尼诱导了IR-ANP浓度的血浆水平显着升高，但其他阿片类肽都没有诱导这种增加。在吗啡和芬太尼基团中观察到血浆周期GMP水平以及IR-ANP的显着增加。循环GMP强烈牵涉到IR-ANP的第二个使者。等离子体周期GMP的增加与血浆IR-ANP水平的增加相关。这些显着增加被纳洛酮完全阻断，纳洛酮是对MU类型的阿片类药物受体的强大拮抗剂。这些结果表明，高剂量的吗啡会通过吗啡受体增加血浆IR-ANP。此外，吗啡和芬太尼观察到了血浆儿茶酚胺（NE和E）的显着增加以及IR-ANP和CGMP。该观察结果将表明内差儿茶酚胺与鸦片受体可能涉及IR-ANP分泌的回流。2）体外实验：大鼠心房细胞是通过心房的酶解离而获得的。将细胞与阿片类肽和儿茶酚胺一起在95％O和5％CO的情况下与38 C孵育4小时。 dynorphin和Catecholamine增加了IR-ANP在培养管培养基中的浓度，但不是另一种肽。特尼酚和儿茶酚胺的组合显着增加了中庭细胞的IR-ANP分泌，尤其是。与多巴胺诱导的10倍相比，IR-ANP中的增长并未被纳洛酮阻塞。这些来自体内的实验和体外的结果表明，内源性儿茶酚胺与大剂量的大剂量诱导的ANP分泌有关。