The role of vasopressin V1a receptor in diabetic nephropathy and the invention of new therapy.

我们报道了加压素V1 a受体缺陷小鼠出现4型肾小管酸中毒，其特征是肾功能降低、代谢性酸中毒和高钾血症。由于集合管是肾脏泌酸的主要场所，我们从SV 40大T抗原Tg大鼠中建立了一种新的闰间细胞系（IN-IC细胞）。利用这些细胞，我们还发现，加压素V1 a受体所需的盐皮质激素受体的核质运输醛固酮在嵌入细胞。总之，血管加压素V1 a受体是必需的酸-碱调节醛固酮在闰细胞。提示加压素V1 a受体拮抗剂有可能作为醛固酮拮抗剂应用于临床。

We reported that vasopressin V1a receptor deficient mice show type 4 renal tubular acidosis, which is characterized by reduced renal function, metabolic acidosis and hyperkalemia. Since the colleting ducts are the main cite of acid secretion by the kidney, we established a new cell line of the intercalated cells(IN-IC cells) from SV40 large T antigen Tg rats. Using these cells, we also found that vasopressin V1a receptor is required for nucleocytoplasmic transport of mineralocorticoid receptor by aldosterone in the intercalated cells. In conclusion, vasopressin V1a receptor is essential for acid-base regulation by aldosterone in intercalated cells. These data suggest the possibility of clinical use of vasopressin V1a receptor antagonist as an aldosterone antagonist.