The role of vasopressin V1a receptor in diabetic nephropathy and the invention of new therapy.
The role of vasopressin V1a receptor in diabetic nephropathy and the invention of new therapy.
批准号:
21591064
负责人:
NONOGUCHI Hiroshi
金额:
$2.91万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
2009
资助国家:
日本
项目状态:
已结题
起止时间:
2009 至 2011
中文摘要
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英文摘要
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.
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Acid decreased the expression of Ca-sensing receptor in type-B of mouse kidney collecting duct intercalated cells
酸降低小鼠肾集合管嵌入细胞B型Ca2+敏感受体的表达
DOI:
--
发表时间:
2011
期刊:
影响因子:
--
作者:
[Yasuoka Y, Sato Y, Izumi Y, Nonoguchi H, Kawahara K]
通讯作者:
Kawahara K
Interaction of aldosterone and vasopressin in the intercalated cells of the collecting ducts
醛固酮和加压素在集合管闰细胞中的相互作用
DOI:
--
发表时间:
2010
期刊:
影响因子:
--
作者:
[Kahori Hori, et al.]
通讯作者:
et al.
Mechanisms of Type 4(hyperkalemic) Renal Tubular Acidosis
4型(高钾血症)肾小管性酸中毒的机制
DOI:
--
发表时间:
2010
期刊:
影响因子:
--
作者:
[Hori K, Nagai T, Izumi Y, Nakayama Y, Hasuike Y, Nanami M, Yasuoka Y, Otaki Y, Tanoue A, Kawahara K, Tomita K, Nakanishi T, Nonoguchi H.]
通讯作者:
Nonoguchi H.
DOI:
10.1001/jama.2010.39
发表时间:
2010-02-03
期刊:
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
影响因子:
120.7
作者:
[Hemmelgarn, Brenda R., Manns, Braden J., Tonelli, Marcello]
通讯作者:
Tonelli, Marcello
DOI:
10.1159/000337742
发表时间:
2012-01-01
期刊:
AMERICAN JOURNAL OF NEPHROLOGY
影响因子:
4.2
作者:
[Moriguchi, Rintarou, Otaki, Yoshinaga, Nakanishi, Takeshi]
通讯作者:
Nakanishi, Takeshi
共 32 条
The mechanisms of regulation of nuclocytoplasmic transport of mineralocorticoid receptor by vasopressin V1a receptor.
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批准号:24591244
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项目类别:Grant-in-Aid for Scientific Research (C)
-
资助金额:$3.41万
-
财政年份:2012
-
负责人:NONOGUCHI Hiroshi
-
依托单位:
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.
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批准号:19590955
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$2.91万
-
财政年份:2007
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负责人:NONOGUCHI Hiroshi
-
依托单位:
Functional analysis of antidiuretic hormone receptor using V1a knockout mice and invention of new diuretics.
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批准号:17590833
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$2.24万
-
财政年份:2005
-
负责人:NONOGUCHI Hiroshi
-
依托单位:
The investigation of the mechanisms and therapy of the abnormality in antidiuretic hormone action in patients with chronic renal failure
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批准号:15590852
-
项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$2.18万
-
财政年份:2003
-
负责人:NONOGUCHI Hiroshi
-
依托单位:
Regulation of diuresis by 2 types of antidiuretic hormone receptor in chronic renal failure and therapeutic investigation of edema
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批准号:13671121
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项目类别:Grant-in-Aid for Scientific Research (C)
-
资助金额:$2.24万
-
财政年份:2001
-
负责人:NONOGUCHI Hiroshi
-
依托单位:
The study on molecular biological mechanisms and therapy of sodiam and acid disturbance in renal failure
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批准号:10671000
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项目类别:Grant-in-Aid for Scientific Research (C)
-
资助金额:$2.24万
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财政年份:1998
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负责人:NONOGUCHI Hiroshi
-
依托单位:
The investigation of molecular biological mechanisms and therapy of refractory renal edema.
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批准号:08671291
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项目类别:Grant-in-Aid for Scientific Research (C)
-
资助金额:$1.41万
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财政年份:1996
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负责人:NONOGUCHI Hiroshi
-
依托单位:
The investigation of the mechanisms and the rapy of renal edema from the acpect of cell porality.
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批准号:06671133
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项目类别:Grant-in-Aid for General Scientific Research (C)
-
资助金额:$1.34万
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财政年份:1994
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负责人:NONOGUCHI Hiroshi
-
依托单位:
海外基金