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
基本信息
- 批准号:15590852
- 负责人:
- 金额:$ 2.18万
- 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:2003
- 资助国家:日本
- 起止时间:2003 至 2004
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
We investigated renal function and abnormality in V1a-knockout mice and found that there is no abnormality in urine concentrating ability. Vasopressin-dependent camp generation in V1a receptor-knockout mice was also not different from control mice. Now, we are investigating V1a receptor transgenic mice.We next investigated urinary excretion of aquaporin-2(AQP2) in rats with metabolic acidosis. Although urinary AQP2 excretion was largely decreased, AQP2 mRNA and protein in outer medullary collecting ducts were increased in rats with metabolic acidosis. These data suggest the presence of abnormality in trafficking of AQP2 from intracellular vesicle to the apical membrane in metabolic acidosis. We observed same tendency in rats with potassium depletion. Since intracellular acidosis is known to occur in metabolic acidosis and potassium depletion, intracellular acidosis may have a key role for the decreased trafficking of AQP2 in the collecting ducts. We are now collaborating with Dr, Nielsen in Aarhus University in Denmark and Dr.knepper in National Institutes of health in USA.
我们研究了v1a基因敲除小鼠的肾功能和异常情况,发现尿浓缩能力没有异常。V1a受体敲除小鼠抗利尿激素依赖性camp的产生也与对照小鼠没有差异。现在,我们正在研究V1a受体转基因小鼠。接下来,我们研究了代谢性酸中毒大鼠尿中水通道蛋白-2(AQP2)的排泄。代谢性酸中毒大鼠尿AQP2排泄量明显减少,但髓外集管AQP2 mRNA和蛋白水平升高。这些数据提示代谢性酸中毒中AQP2从胞内囊泡转运到顶膜存在异常。我们在缺钾大鼠中观察到同样的趋势。由于已知细胞内酸中毒发生在代谢性酸中毒和钾耗竭中,细胞内酸中毒可能是集管中AQP2转运减少的关键作用。我们现在正与丹麦奥胡斯大学的Nielsen博士和美国国立卫生研究院的knepper博士合作。
项目成果
期刊论文数量(42)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Two male siblings with hereditary renal hypouricemia and exercise-induced ARF
- DOI:10.1053/j.ajkd.2003.08.032
- 发表时间:2003-12-01
- 期刊:
- 影响因子:13.2
- 作者:Tanaka, M;Itoh, K;Tomita, K
- 通讯作者:Tomita, K
Machida K: "Acute regulation of the eoithelial sodium channel gene by vasopressin and hyperosmolality"Hypertens Res. 26・8. 629-634 (2003)
Machida K:“加压素和高渗透压对上皮钠通道基因的急性调节”Hypertens Res 26・8(2003)。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Gene regulation of renal-osmotic stress-induced Na-Cl organic solute cotransporter.
肾渗透应激诱导的 Na-Cl 有机溶质协同转运蛋白的基因调控。
- DOI:
- 发表时间:2004
- 期刊:
- 影响因子:0
- 作者:Tuyen do G;Kitamura K;Adachi M;Miyoshi T;Wakida N;Nagano J;Nonoguchi H;Tomita K.;Tuyen do G.;Baba T
- 通讯作者:Baba T
Angiotensin-converting enzyme inhibitor withdrawal and ACE gene polymorphism.
血管紧张素转换酶抑制剂戒断与ACE基因多态性。
- DOI:
- 发表时间:2003
- 期刊:
- 影响因子:0
- 作者:Nonoguchi H;Kiyama S;Inoue H;Nakayama Y;Inoue T;Kohda Y;Machida K;Tajima A;Kitamura K;Miyoshi T;Shimada H;Shimada H;Tajiri M;Honda Y;Tanaka M;Tomita K.
- 通讯作者:Tomita K.
Baba T: "Gene Regulation of Renal Osmotic Stress-induced Na-Cl Organic Solute Cotransporter (ROSIT)"Nephron Exp Nephrol. (in press).
Baba T:“肾渗透应激诱导的 Na-Cl 有机溶质协同转运蛋白 (ROSIT) 的基因调节”Nephron Exp Nephrol。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
{{
item.title }}
{{ item.translation_title }}
- DOI:
{{ item.doi }} - 发表时间:
{{ item.publish_year }} - 期刊:
- 影响因子:{{ item.factor }}
- 作者:
{{ item.authors }} - 通讯作者:
{{ item.author }}
数据更新时间:{{ journalArticles.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ monograph.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ sciAawards.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ conferencePapers.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ patent.updateTime }}
NONOGUCHI Hiroshi其他文献
NONOGUCHI Hiroshi的其他文献
{{
item.title }}
{{ item.translation_title }}
- DOI:
{{ item.doi }} - 发表时间:
{{ item.publish_year }} - 期刊:
- 影响因子:{{ item.factor }}
- 作者:
{{ item.authors }} - 通讯作者:
{{ item.author }}
{{ 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:
$ 2.18万 - 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:
$ 2.18万 - 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:
$ 2.18万 - 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:
$ 2.18万 - 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:
$ 2.18万 - 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:
$ 2.18万 - 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:
$ 2.18万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
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 - 财政年份:1994
- 资助金额:
$ 2.18万 - 项目类别:
Grant-in-Aid for General Scientific Research (C)
相似海外基金
Elucidation of the mechanism of V1a receptor-induced uterine contraction via receptor coordination and derivation of therapeutic targets for preterm birth
通过受体协调阐明 V1a 受体诱导子宫收缩的机制并推导早产治疗靶点
- 批准号:
21K09477 - 财政年份:2021
- 资助金额:
$ 2.18万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Role of arginine-vasopressin and V1A receptor in psychosocial stress-induced myocardial injury
精氨酸加压素和 V1A 受体在心理应激诱发的心肌损伤中的作用
- 批准号:
10671052 - 财政年份:2021
- 资助金额:
$ 2.18万 - 项目类别:
Role of arginine-vasopressin and V1A receptor in psychosocial stress-induced myocardial injury
精氨酸加压素和 V1A 受体在心理应激诱发的心肌损伤中的作用
- 批准号:
10283131 - 财政年份:2021
- 资助金额:
$ 2.18万 - 项目类别:
Role of arginine-vasopressin and V1A receptor in psychosocial stress-induced myocardial injury
精氨酸加压素和 V1A 受体在心理应激诱发的心肌损伤中的作用
- 批准号:
10470346 - 财政年份:2021
- 资助金额:
$ 2.18万 - 项目类别:
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:
$ 2.18万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
A role of V1a receptor in water/electrolytes metabolism.
V1a 受体在水/电解质代谢中的作用。
- 批准号:
24790222 - 财政年份:2012
- 资助金额:
$ 2.18万 - 项目类别:
Grant-in-Aid for Young Scientists (B)
Vasopressin V1a receptor gene and adherence to an exercise program: the congenital and acquired mechanisms
加压素 V1a 受体基因和坚持锻炼计划:先天性和后天性机制
- 批准号:
24689014 - 财政年份:2012
- 资助金额:
$ 2.18万 - 项目类别:
Grant-in-Aid for Young Scientists (A)
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:
$ 2.18万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
AAV MEDIATED TRANSFER OF V1A RECEPTOR GENE IN ADULT CNS
AAV 介导的成人 CNS 中 V1A 受体基因的转移
- 批准号:
6186370 - 财政年份:1999
- 资助金额:
$ 2.18万 - 项目类别:
AAV MEDIATED TRANSFER OF V1A RECEPTOR GENE IN ADULT CNS
AAV 介导的成人 CNS 中 V1A 受体基因的转移
- 批准号:
2850630 - 财政年份:1999
- 资助金额:
$ 2.18万 - 项目类别: