The investigation of the mechanisms and the rapy of renal edema from the acpect of cell porality.

从细胞多孔性角度探讨肾水肿发生机制及治疗方法。

• 批准号: 06671133
• 负责人: NONOGUCHI Hiroshi
• 金额: $ 1.34万
• 依托单位: Kumamoto University (1995)Tokyo Medical and Dental University (1994)
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (C)
• 财政年份: 1994
• 资助国家: 日本
• 起止时间: 1994 至 1995
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-06671133/
• 关键词: antidiuretic hormone; V_2 receptor; V_1a receptor; edema; inner medullary collecting duct; chronic renal failure; vasopressin (AVP); Vlaレセプター; V2(AOP)レセプター; 細胞極性

We investigated immunohistochemical localization of V2 vasopressin (antidiuretic hormone) receptor along the nephron using a specific polyclonal antibody. V2 receptor was present in some of thick ascending limbs and all of pricipal and inner medullary collecting duct (IMCD) cells. Not only basolateral but also luminal membrane was stained by the antibody in collecting ducts, especially in terminal IMCD.Therefore, to learn the functional role of luminal V2 receptor in terminal IMCD,we investigated the luminal effects of vasopressin on osmotic water permeability (Pf), urea permeability (Pu), and cAMP accumulation using isolated perfused rat terminal IMCD.Luminal vasopressin caused a small increase in cAMP accumulation, Pf and Pu in the absence of bath vasopressin. In contrast, luminal vasopressin inhibited Pf and Pu by 30-65% in the presence of bath vasopressin by decreasing cAMP accumulation via V1a or oxytocin receptors and by an unknown mechanism via V2 receptors in the luminal membrane of terminal IMCD.Therefore, luminal vasopressin acts as an diuretic hormone rather than antidiuretic hormone in terminal IMCD.

我们使用特定的多克隆抗体研究了V2加压素（抗利尿激素）受体的免疫组织化学定位。 V2受体存在于某些较厚的上升肢，以及所有的胸腔和内部髓质收集管（IMCD）细胞中。抗体在收集管道中，尤其是在末端IMCD中染色，不仅会受到抗体的染色。因此，要学习腔内V2受体在末端IMCD中的功能作用，我们研究了血管联蛋白对渗透性水的渗透性（PF）的延伸（PF）的腔仪（PU）的腔内作用，并研究在没有浴加压素的情况下，血管加压素导致营地积聚，PF和PU的增加。相反，在存在沐浴加压素的情况下，腔血管加压素通过通过V1A或催产素受体减少营地积累，并通过通过V2受体在末端IMCD的腔膜上通过V2受体来抑制PF和PU，抑制PF，并抑制PF。

项目成果

T.Shiigai,H.Nonoguchi,K.Tomita: "Dietary protein restriction and blood-pressue control in chron:c renal inaufficieney" N.Engl.J.Med.331. 405-406 (1994)

T.Shiigai、H.Nonoguchi、K.Tomita：“慢性肾功能不全中的饮食蛋白质限制和血压控制”N.Engl.J.Med.331。

Y.Terada,et al.: "Sequential activation of Raf-1 kinase,mitogen-activots protein (MAP) kinase kinase,MAP kinase,and S6 kinaseby hyperosmolalily in renol cells" J.Biol.Chem.268. 31296-31301 (1994)

Y.Terada 等人：“Raf-1 激酶、丝裂原激活蛋白 (MAP) 激酶激酶、MAP 激酶和 S6 激酶在肾醇细胞中通过高渗透压的顺序激活”J.Biol.Chem.268。

Y.Terada,et al.: "Presence and requlation of RAF-1-K(Kinase). MAPK-K,MAP-K,and S6-K in rat nephon segments." J.Am.Soc.Nephrol.6. 1566-1577 (1995)

Y.Terada 等人：“大鼠肾段中 RAF-1-K（激酶）、MAPK-K、MAP-K 和 S6-K 的存在和调节。”

M.Yoshida,H.Nonoguchi,et al: "Three cases of morlignant hypertenson:the roles of endothelin-1 and the renin-angiotensin-aldoterone sptem." Clin.Nephrol.42. 295-299 (1994)

M.Yoshida，H.Nonoguchi，等人：“死亡性高血压三例：内皮素-1 和肾素-血管紧张素-醛酮系统的作用”。

T.Shiigai, H.Nonoguchi, K.Tomita.: "Dietary protein restriction and blood-pressure control in chronic renal insufficiency." N.Engl.J.Med.331. 405-406 (1994)

T.Shiigai、H.Nonoguchi、K.Tomita.：“慢性肾功能不全的饮食蛋白质限制和血压控制。”