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。
基本信息
- 批准号:06671133
- 负责人:
- 金额:$ 1.34万
- 依托单位:
- 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:
- 关键词:
项目摘要
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.
我们利用特异性多克隆抗体研究了V2抗利尿激素受体沿肾元的免疫组织化学定位。部分粗升肢及所有髓内集管(IMCD)细胞均可见V2受体。在收集管中,抗体不仅可以染色基底外膜,而且可以染色管腔膜,特别是在终末IMCD中。因此,为了了解管腔V2受体在终末IMCD中的功能作用,我们利用离体灌注大鼠终末IMCD研究加压素对渗透水通透性(Pf)、尿素通透性(Pu)和cAMP积累的管腔影响。在没有盆腔加压素的情况下,腔内加压素引起cAMP积累、Pf和Pu的小幅增加。相比之下,管腔加压素通过V1a或催产素受体减少cAMP的积累,以及通过终末IMCD管腔膜中V2受体的未知机制,在盆腔加压素存在的情况下抑制Pf和Pu的30-65%。因此,腔内加压素在晚期IMCD中作为利尿激素而不是抗利尿激素。
项目成果
期刊论文数量(44)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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。
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- 影响因子:0
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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。”
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- 影响因子:0
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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。
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- 影响因子:0
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A.Owada,: "Endothelin(ET)-3 stimulates cyclic guanosine 3,5-monophosphate production via ET_B receptor by producing nitric oxide in isolated rat glomerulus, and in cultured rat mesangial cells." J. Clin. Invest.93. 556-563 (1994)
A.Owada:“内皮素 (ET)-3 通过 ET_B 受体在离体大鼠肾小球和培养的大鼠肾小球膜细胞中产生一氧化氮,从而刺激环鸟苷 3,5-单磷酸的产生。”
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- 影响因子:0
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- 通讯作者:
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。”
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NONOGUCHI Hiroshi其他文献
NONOGUCHI Hiroshi的其他文献
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{{ truncateString('NONOGUCHI Hiroshi', 18)}}的其他基金
The mechanisms of regulation of nuclocytoplasmic transport of mineralocorticoid receptor by vasopressin V1a receptor.
加压素 V1a 受体调节盐皮质激素受体核细胞质转运的机制。
- 批准号:
24591244 - 财政年份:2012
- 资助金额:
$ 1.34万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
The role of vasopressin V1a receptor in diabetic nephropathy and the invention of new therapy.
加压素V1a受体在糖尿病肾病中的作用及新疗法的发明。
- 批准号:
21591064 - 财政年份:2009
- 资助金额:
$ 1.34万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
The investigation of the role of interaction of two types of antidiuretic hormone receptors for diuresis and the invention of the new therapy for renal edema.
研究两类抗利尿激素受体相互作用对利尿的作用并发明治疗肾水肿的新疗法。
- 批准号:
19590955 - 财政年份:2007
- 资助金额:
$ 1.34万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Functional analysis of antidiuretic hormone receptor using V1a knockout mice and invention of new diuretics.
V1a基因敲除小鼠抗利尿激素受体功能分析及新型利尿剂的发明。
- 批准号:
17590833 - 财政年份:2005
- 资助金额:
$ 1.34万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
The investigation of the mechanisms and therapy of the abnormality in antidiuretic hormone action in patients with chronic renal failure
慢性肾功能衰竭患者抗利尿激素作用异常的机制及治疗探讨
- 批准号:
15590852 - 财政年份:2003
- 资助金额:
$ 1.34万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Regulation of diuresis by 2 types of antidiuretic hormone receptor in chronic renal failure and therapeutic investigation of edema
2种抗利尿激素受体对慢性肾功能衰竭利尿的调节及水肿治疗研究
- 批准号:
13671121 - 财政年份:2001
- 资助金额:
$ 1.34万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
The study on molecular biological mechanisms and therapy of sodiam and acid disturbance in renal failure
肾衰竭钠酸紊乱的分子生物学机制及治疗研究
- 批准号:
10671000 - 财政年份:1998
- 资助金额:
$ 1.34万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
The investigation of molecular biological mechanisms and therapy of refractory renal edema.
难治性肾水肿的分子生物学机制及治疗研究。
- 批准号:
08671291 - 财政年份:1996
- 资助金额:
$ 1.34万 - 项目类别:
Grant-in-Aid for Scientific Research (C)