Zingg H H
Department of Medicine, Royal Victoria Hospital, McGill University, Montreal, Quebec, Canada.
Baillieres Clin Endocrinol Metab. 1996 Jan;10(1):75-96. doi: 10.1016/s0950-351x(96)80314-4.
The oxytocin and the vasopressin V1a, V1b and V2 receptors have recently been cloned and shown to form a sub-family within the large superfamily of G-protein-linked receptors. Renal V2 receptors mediate vasopressin-induced water reabsorption via induction of intracellular cAMP production in collecting duct cells. Most remaining actions of vasopressin on blood vessel constriction, liver glycogenolysis, platelet adhesion, adrenal angiotensin II secretion and certain brain functions are mediated via v1a-type receptors that are coupled to a Gq/11 protein. V1 receptor activation leads to stimulation of phospholipases C, D and A2 and an increase in intracellular calcium. Vasopressin stimulates pituitary corticotrophin release via a third vasopressin receptor type (V1b) which is present on corticotrophs. Oxytocin induces myometrial contraction, endometrial prostaglandin F2 alpha production, mammary gland milk ejection, renal natriuresis and specific sexual, affiliative and maternal behaviours via oxytocin receptors which are also coupled to a Gq/11 protein. Although only one oxytocin receptor type has been cloned so far, recent binding studies indicate that uterine endometrial oxytocin receptors may constitute a distinct receptor subtype. In contrast to most other membrane receptors, the expression of oxytocin receptors undergoes very rapid and physiologically relevant up-and-down-regulation. A > 100-fold up-regulation of uterine oxytocin receptors occurs during gestation and may represent the trigger for parturition. Indeed, oxytocin receptor antagonists are able to counteract preterm labour and may soon be available for clinical use. The presence of oxytocin receptors on breast cancer cells and the growth-inhibitory effects of OT suggest a potential use of oxytocin analogues for breast cancer treatment. Whereas no mutations of the oxytocin or V1a or V1b receptors have been found, over 60 different genetic mutations of the (renal) V2 receptor have been described which represent the cause for congenital nephrogenic diabetes insipidus.
催产素以及血管加压素V1a、V1b和V2受体最近已被克隆，并显示在G蛋白偶联受体的大型超家族中形成一个亚家族。肾脏V2受体通过诱导集合管细胞内cAMP产生来介导血管加压素诱导的水重吸收。血管加压素对血管收缩、肝糖原分解、血小板黏附、肾上腺血管紧张素II分泌和某些脑功能的大多数其余作用是通过与Gq/11蛋白偶联的V1a型受体介导的。V1受体激活导致磷脂酶C、D和A2的刺激以及细胞内钙的增加。血管加压素通过存在于促肾上腺皮质激素细胞上的第三种血管加压素受体类型（V1b）刺激垂体促肾上腺皮质激素释放。催产素通过同样与Gq/11蛋白偶联的催产素受体诱导子宫肌层收缩、子宫内膜前列腺素F2α产生、乳腺排乳、肾排钠以及特定的性行为、亲和行为和母性行为。尽管到目前为止只克隆了一种催产素受体类型，但最近的结合研究表明，子宫内膜催产素受体可能构成一种独特的受体亚型。与大多数其他膜受体不同，催产素受体的表达经历非常快速且与生理相关的上调和下调。妊娠期间子宫催产素受体上调超过100倍，可能是分娩的触发因素。事实上，催产素受体拮抗剂能够抵消早产，可能很快可供临床使用。乳腺癌细胞上存在催产素受体以及催产素的生长抑制作用表明催产素类似物在乳腺癌治疗中具有潜在用途。虽然未发现催产素或V1a或V1b受体的突变，但已描述了（肾脏）V2受体的60多种不同基因突变，这些突变是先天性肾性尿崩症的病因。
