{"title":"多巴胺和前列腺素对血管去甲肾上腺素反应的相互作用:多巴胺抑制PGE1的作用","authors":"M. Oka, M.S. Manku, D.F. Horrobin","doi":"10.1016/0161-4630(81)90132-4","DOIUrl":null,"url":null,"abstract":"<div><p>Interactions between dopamine and responses to noradrenaline as modulated by prostaglandins (PGs) were studied in the perfused rat mesenteric vascular bed. When perfused alone dopamine up to a concentration of 10<sup>−7</sup>M neither changed baseline pressure nor modified the pressor response to noradrenaline. Dopamine at 10<sup>−9</sup> to 10<sup>−7</sup>M significantly inhibited responses to noradrenaline which had been enhanced by the presence of 10<sup>−10</sup> to 10<sup>−8</sup> M PGEI. In preparations in which vascular responses to noradrenaline had been abolised by indomethacin and restored by adding PGEI, 10<sup>−9</sup> to 1<sup>−7</sup>M dopamine significantly inhibited the restored responses. Dopamine also attenuated the inhibitory effects of prostacyclin on pressor responses to noradrenaline but it did not change the actions of either PGE2 or PGF2 alpha. Pimozide, a mainly centrally acting dopamine antagonist, did not interfere with these peripheral actions of dopamine. The dopamine effects were blocked by another dopamine antagonist, metoclopramide. Dopamine can inhibit the effects of PGEI and prostacyclin in the rat mesenteric vascular bed, possibly by interacting with specific dopamine receptors.</p></div>","PeriodicalId":76381,"journal":{"name":"Prostaglandins and medicine","volume":"7 4","pages":"Pages 267-280"},"PeriodicalIF":0.0000,"publicationDate":"1981-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0161-4630(81)90132-4","citationCount":"4","resultStr":"{\"title\":\"Interactions between dopamine and prostaglandins on vascular reactivity to noradrenaline: Dopamine inhibits the action of PGE1\",\"authors\":\"M. Oka, M.S. Manku, D.F. Horrobin\",\"doi\":\"10.1016/0161-4630(81)90132-4\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>Interactions between dopamine and responses to noradrenaline as modulated by prostaglandins (PGs) were studied in the perfused rat mesenteric vascular bed. When perfused alone dopamine up to a concentration of 10<sup>−7</sup>M neither changed baseline pressure nor modified the pressor response to noradrenaline. Dopamine at 10<sup>−9</sup> to 10<sup>−7</sup>M significantly inhibited responses to noradrenaline which had been enhanced by the presence of 10<sup>−10</sup> to 10<sup>−8</sup> M PGEI. In preparations in which vascular responses to noradrenaline had been abolised by indomethacin and restored by adding PGEI, 10<sup>−9</sup> to 1<sup>−7</sup>M dopamine significantly inhibited the restored responses. Dopamine also attenuated the inhibitory effects of prostacyclin on pressor responses to noradrenaline but it did not change the actions of either PGE2 or PGF2 alpha. Pimozide, a mainly centrally acting dopamine antagonist, did not interfere with these peripheral actions of dopamine. The dopamine effects were blocked by another dopamine antagonist, metoclopramide. Dopamine can inhibit the effects of PGEI and prostacyclin in the rat mesenteric vascular bed, possibly by interacting with specific dopamine receptors.</p></div>\",\"PeriodicalId\":76381,\"journal\":{\"name\":\"Prostaglandins and medicine\",\"volume\":\"7 4\",\"pages\":\"Pages 267-280\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1981-10-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1016/0161-4630(81)90132-4\",\"citationCount\":\"4\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Prostaglandins and medicine\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/0161463081901324\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Prostaglandins and medicine","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/0161463081901324","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 4
摘要
在灌注的大鼠肠系膜血管床上研究了前列腺素(pg)调节的多巴胺与去甲肾上腺素反应之间的相互作用。当单独灌注10−7M浓度的多巴胺时,既没有改变基线血压,也没有改变去甲肾上腺素的升压反应。多巴胺在10−9至10−7M时显著抑制了去甲肾上腺素的反应,而10−10至10−8 M PGEI的存在增强了去甲肾上腺素的反应。在用吲哚美辛消除血管对去甲肾上腺素的反应并通过添加PGEI恢复的制剂中,10−9至1−7M多巴胺显著抑制了血管对去甲肾上腺素的反应。多巴胺也减弱了前列环素对去甲肾上腺素加压反应的抑制作用,但它没有改变PGE2或PGF2 α的作用。吡莫齐特是一种主要的中枢作用多巴胺拮抗剂,不干扰多巴胺的这些外周作用。多巴胺的作用被另一种多巴胺拮抗剂甲氧氯普胺阻断。多巴胺可以抑制PGEI和前列环素在大鼠肠系膜血管床中的作用,可能与特定的多巴胺受体相互作用。
Interactions between dopamine and prostaglandins on vascular reactivity to noradrenaline: Dopamine inhibits the action of PGE1
Interactions between dopamine and responses to noradrenaline as modulated by prostaglandins (PGs) were studied in the perfused rat mesenteric vascular bed. When perfused alone dopamine up to a concentration of 10−7M neither changed baseline pressure nor modified the pressor response to noradrenaline. Dopamine at 10−9 to 10−7M significantly inhibited responses to noradrenaline which had been enhanced by the presence of 10−10 to 10−8 M PGEI. In preparations in which vascular responses to noradrenaline had been abolised by indomethacin and restored by adding PGEI, 10−9 to 1−7M dopamine significantly inhibited the restored responses. Dopamine also attenuated the inhibitory effects of prostacyclin on pressor responses to noradrenaline but it did not change the actions of either PGE2 or PGF2 alpha. Pimozide, a mainly centrally acting dopamine antagonist, did not interfere with these peripheral actions of dopamine. The dopamine effects were blocked by another dopamine antagonist, metoclopramide. Dopamine can inhibit the effects of PGEI and prostacyclin in the rat mesenteric vascular bed, possibly by interacting with specific dopamine receptors.