Goiny M, Uvnäs-Moberg K
Peptides. 1986;7 Suppl 1:221-4. doi: 10.1016/0196-9781(86)90189-0.
The effects of some dopaminomimetics on VIP levels in peripheral venous blood of conscious dogs were analysed with a radioimmunoassay. The dopamine D2 agonist pergolide, like apomorphine and bromocriptine, increased VIP levels. The putative DA autoreceptor agonist 3PPP, as well as the D1 agonist SK&F 38393 were devoid of action. The D1 antagonist SCH 23390 did not abolish the effect of apomorphine. It is suggested that monitoring of VIP levels could be an interesting screening test for activity at D2 receptors. Amphetamine did not modify VIP levels suggesting that DA neurons are not involved in the mechanism leading to a release of VIP. The VIP response to apomorphine was not suppressed by an infusion of somatostatin. Decreasing blood pressure with nitroglycerin or with the adrenergic antagonist prazosin did not release VIP. The mechanism by which administration of dopaminomimetics lead to a release of VIP is further discussed.
采用放射免疫分析法分析了某些多巴胺模拟物对清醒犬外周静脉血中血管活性肠肽（VIP）水平的影响。多巴胺D2激动剂培高利特，与阿扑吗啡和溴隐亭一样，可提高VIP水平。假定的多巴胺自身受体激动剂3PPP以及D1激动剂SK&F 38393则无此作用。D1拮抗剂SCH 23390并未消除阿扑吗啡的作用。提示监测VIP水平可能是一种有趣的D2受体活性筛选试验。苯丙胺未改变VIP水平，提示多巴胺能神经元不参与导致VIP释放的机制。生长抑素输注并未抑制阿扑吗啡引起的VIP反应。用硝酸甘油或肾上腺素能拮抗剂哌唑嗪降低血压并未释放VIP。文中进一步讨论了给予多巴胺模拟物导致VIP释放的机制。
