Pettibone D J, Mueller G P
Brain Res. 1981 Sep 28;221(2):409-14. doi: 10.1016/0006-8993(81)90792-7.
Clonidine (10(-6), 10(-7) M) evokes the release of beta endorphin-like immunoreactivity (beta-END-LI) from cell cultures of anterior (pars distalis) but not neurointermediate (pars nervosa plus pars intermedia) lobe of the rat pituitary. This drug-induced secretion is blocked by alpha-adrenergic (phenoxybenzamine, yohimbine; 10(-5) M) but not beta-adrenergic (propranolol, 10(-5) M) antagonism. Gel filtration (Sephadex G-50) reveals that beta-END-LI released from anterior lobe cells consists of 2 major forms of immunoreactivity which coelute with beta-lipotropin or beta-endorphin standards. Conversely, beta-END-LI released spontaneously from neurointermediate lobe cells almost entirely corresponds to beta-endorphin. The data show that alpha-adrenergic stimulation by clonidine releases beta-END-LI selectively from cells of anterior but not neurointermediate lobe in vitro and suggests that the clonidine-induced release of pituitary beta-END-LI we have observed in vivo occurs in part by direct action on the corticotrophs of the pars distalis.
可乐定(10⁻⁶、10⁻⁷M)可促使大鼠垂体前叶(远侧部)而非神经中间叶(神经垂体加中间部)细胞培养物释放β-内啡肽样免疫反应性物质(β-END-LI)。这种药物诱导的分泌可被α-肾上腺素能拮抗剂(酚苄明、育亨宾;10⁻⁵M)阻断,但不能被β-肾上腺素能拮抗剂(普萘洛尔,10⁻⁵M)阻断。凝胶过滤(葡聚糖凝胶G-50)显示,前叶细胞释放的β-END-LI由两种主要的免疫反应性形式组成,它们与β-促脂素或β-内啡肽标准品共洗脱。相反,神经中间叶细胞自发释放的β-END-LI几乎完全对应于β-内啡肽。数据表明,可乐定对α-肾上腺素能的刺激在体外可选择性地从前叶而非神经中间叶细胞释放β-END-LI,并提示我们在体内观察到的可乐定诱导的垂体β-END-LI释放部分是通过直接作用于远侧部的促肾上腺皮质激素细胞而发生的。