Jans D A, Pavo I, Fahrenholz F
Max-Planck-Institut für Biophysik, Frankfurt am Main, Germany.
FEBS Lett. 1993 Jan 4;315(2):134-8. doi: 10.1016/0014-5793(93)81149-t.
Using a variety of peptide analogues of oxytocin (OT) and Arg8-vasopressin (AVP), OT-mediated induction of urokinase-type plasminogen activator (uPA) was examined in LLC-PK1 renal epithelial cells, which possess distinct high-affinity receptors of both the OT- and vasopressin renal (V2-) types. OT or OT-receptor specific agonists induced concentration-dependent cAMP synthesis, activation of the cAMP-dependent protein kinase (cAMP-PK) and uPA production consistent with their respective binding affinities for the V2- and not the OT-receptor. OT-mediated uPA induction could be inhibited in a concentration-dependent fashion by coincubation with a V2/V1-receptor specific antagonist, but not by an OT-receptor specific antagonist. Results implied that stimulation of cAMP- and uPA responses in LLC-PK1 cells by OT was V2-receptor-mediated.
利用多种催产素（OT）和精氨酸8-加压素（AVP）的肽类似物，在LLC-PK1肾上皮细胞中检测了OT介导的尿激酶型纤溶酶原激活剂（uPA）的诱导情况，该细胞具有OT型和加压素肾型（V2-）两种不同的高亲和力受体。OT或OT受体特异性激动剂诱导浓度依赖性的cAMP合成、cAMP依赖性蛋白激酶（cAMP-PK）的激活以及uPA的产生，这与其对V2-受体而非OT受体的各自结合亲和力一致。通过与V2/V1受体特异性拮抗剂共同孵育，OT介导的uPA诱导可被浓度依赖性抑制，但不能被OT受体特异性拮抗剂抑制。结果表明，OT对LLC-PK1细胞中cAMP和uPA反应的刺激是由V2受体介导的。
