2001 Fiscal Year Final Research Report Summary
Regulation of Na-transporters by steroid hormones : genomic and non-genomic actions
| Project/Area Number |
11671043
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | Jichi Medical School |
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Principal Investigator |
MUTO Shigeaki Jichi Medical School, Dept Nephrol, Assistant Professor, 医学部, 講師 (40190855)
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| Co-Investigator(Kenkyū-buntansha) |
EBATA Satoru Jichi Medical School, Dept Nephrol, Instructor, 医学部, 助手 (70265247)
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| Project Period (FY) |
1999 – 2001
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| Keywords | Na pump / Na / H exchange / epithelial Na channel / mineralocorticoid / glucocorticoid / membrane crosstalk / glucocorticoid surface receptor |
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| Research Abstract |
We used the cortical collecting duct (CCD) from rabbit kidneys and cultured vascular smooth muscle cells (VSMC) to determine the effects of steroid hormones on Na-transporters (Na pump, Na/H exchanger, and epithelial Na channel) in terms of their genomic and non-genomic actions. The results were in the following :
1) In the CCD, acute elevation of basolateral K concentrations from 2.5 to 8.5 mM activated the basolateral Na pump, which secondarily elevates the apical Na and K conductances. DOCA pretreatment increased the basolateral K conductances and augmented the response to the rise of K of both the basolateral Na pump activity and the apical cation conductances. Luminal Na concentration, by changes in cell Na concentrations, modulated the tight coupling between the basolateral Na pump and apical cation conductances; 2) In the CCD from control rabbits, raising luminal Na concentrations from 14 to 147 mM activated basolateral Na pump and apical Na and K conductances via increased cell Na concentrations. The luminal Na-dependent activation of the basolateral pump and the apical cation conductances was sharply enhanced in the CCD from DOCA-treated rabbits. Chronic DOCA pretreatment also increased basolateral K conductance upon raising luminal Na concentration; 3) In VSMC, aldosterone activated Na/H exchange (NHE) by nongenomic and genomic mechanisms; 4) In VSMC, corticosterone activated NHE by nongenomic mechanisms, but inhibited it, by genomic mechanisms.
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