Jones T H, Brown B L, Dobson P R
University Department of Medicine, Northern General Hospital, Sheffield, UK.
Acta Endocrinol (Copenh). 1990 Jul;123(1):37-42. doi: 10.1530/acta.0.1230037.
The effect of the kinin, kallidin (lysyl-bradykinin) on phosphoinositide metabolism and prolactin secretion was examined in male rat anterior pituitary cells in primary culture. Kallidin was found to stimulate both total inositol phosphate production and prolactin release. The stimulation of inositol phosphate was biphasic in nature, similar to that previously reported for bradykinin, although kallidin was approximately 10-fold more potent. Kallidin also stimulated prolactin secretion provoking a maximal stimulation of 193.0 +/- 11.1 (sem)% at 1 mumol/l. These findings suggest that kallidin-induced prolactin secretion may be mediated intracellularly by activation of phosphoinositide metabolism. The B2 receptor antagonists had no significant inhibitory effects on kallidin-stimulated phosphoinositide metabolism or prolactin release. The B1 agonist des-Arg9-bradykinin has previously been shown to have no effect on either parameter. As the effects of kinins on anterior pituitary cells do not appear to be mediated by either of the known kinin receptors, they may, therefore, act via a hitherto unrecognised kinin receptor.
在原代培养的雄性大鼠垂体前叶细胞中，研究了激肽缓激肽释放酶（赖氨酰缓激肽）对磷酸肌醇代谢和催乳素分泌的影响。发现缓激肽释放酶可刺激总肌醇磷酸生成及催乳素释放。肌醇磷酸的刺激呈双相性，与先前报道的缓激肽相似，不过缓激肽释放酶的效力约为缓激肽的10倍。缓激肽释放酶还刺激催乳素分泌，在1 μmol/l时引发的最大刺激为193.0±11.1（标准误）%。这些发现表明，缓激肽释放酶诱导的催乳素分泌可能通过磷酸肌醇代谢的激活在细胞内介导。B2受体拮抗剂对缓激肽释放酶刺激的磷酸肌醇代谢或催乳素释放无显著抑制作用。B1激动剂去精氨酸9 - 缓激肽先前已被证明对这两个参数均无影响。由于激肽对垂体前叶细胞的作用似乎并非由任何一种已知的激肽受体介导，因此它们可能通过一种迄今未被识别的激肽受体发挥作用。
