Suppr超能文献

垂体前叶促肾上腺皮质激素细胞上一种新型的血管加压素受体?

A novel type of vasopressin receptor on anterior pituitary corticotrophs?

作者信息

Baertschi A J, Friedli M

出版信息

Endocrinology. 1985 Feb;116(2):499-502. doi: 10.1210/endo-116-2-499.

Abstract

Suspensions of rat anterior pituitary cells were exposed to corticotropin-releasing factor (CRF) (5 nM) and various neurohormones (0.002-1000 nM). CRF-induced secretion of ACTH was doubled by 0.1 nM arginine vasopressin (AVP), 0.2 nM arginine vasotocin, 1 nM oxytocin, 10 nM angiotensin II, and 100 nM noradrenalin; vasoactive intestinal peptide had no effect at 0.2-200 nM. CRF potentiation by AVP was also observed at lower concentrations of CRF. Since AVP appeared to be the most potent modulator of CRF-induced ACTH secretion, potentiation was further tested with specific antidiuretic and oxytocic agonists. Potentiation was clearly related to pressor biological activity, less so to antidiuretic, and hardly at all to oxytocic activities. However, even at 200 nM, the antipressor antagonists dPTyr(Me)AVP and d(CH2)5Tyr(Me)AVP had no effect on potentiation by AVP. The lack of antagonism was partly due to the agonistic effects of the antagonists on the pituitary gland, an effect not observed within vascular tissue. The results thus suggest that anterior pituitary vasopressin receptors resemble, but are not identical to, V1 (pressor and hepatic), do not resemble the V2 (renal), and might be classified as V3 (pituitary) receptors.

摘要

将大鼠垂体前叶细胞悬液暴露于促肾上腺皮质激素释放因子(CRF)(5 nM)和各种神经激素(0.002 - 1000 nM)中。0.1 nM精氨酸加压素(AVP)、0.2 nM精氨酸催产素、1 nM催产素、10 nM血管紧张素II和100 nM去甲肾上腺素可使CRF诱导的促肾上腺皮质激素(ACTH)分泌增加一倍;0.2 - 200 nM的血管活性肠肽无作用。在较低浓度的CRF时也观察到AVP对CRF的增强作用。由于AVP似乎是CRF诱导ACTH分泌的最有效调节剂,因此用特定的抗利尿和催产激动剂进一步测试了增强作用。增强作用显然与升压生物活性有关,与抗利尿活性关系较小,与催产活性几乎无关。然而,即使在200 nM时,抗升压拮抗剂dPTyr(Me)AVP和d(CH2)5Tyr(Me)AVP对AVP的增强作用也没有影响。缺乏拮抗作用部分是由于拮抗剂对垂体的激动作用,这种作用在血管组织中未观察到。因此,结果表明垂体前叶加压素受体与V1(升压和肝脏)受体相似,但不完全相同,与V2(肾脏)受体不同,可能可归类为V3(垂体)受体。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验