1993 Fiscal Year Final Research Report Summary
The roles of endothelin and growth factors in ischemic acute renal failure.
| Project/Area Number |
04670385
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Fisheries chemistry
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| Research Institution | Hamamatsu University School of Medicine |
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Principal Investigator |
HISHIDA Akira Hamamatsu University School of Medicine, Medicine, Associate Professor, 医学部, 助教授 (70111812)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAMOTO Tatsuo Hamamatsu University School of Medicine, Medicine, Assistant Professor, 医学部, 講師 (30200819)
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| Project Period (FY) |
1992 – 1993
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| Keywords | acute renal failure / nephrectomy / endothelin / thromboxane |
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| Research Abstract |
The roles of endothelin and thromboxane A2 in ischemic acute renal failure were evaluated in rats. A 60 min left renal artery occlusion induced a decrease in inulin clearance(Cin) in left kidney and histological changes including tubular necrosis and cast formation. Antecedent nephrectomy of right kidney attenuates the decrease in Cin and tubular necrosis at 48 hours after ischemia. The beneficial effects of right nephrectomy was associated with the attenuation of the increases in renal endothelin and thromboxane B2 contents. The treatment with monoclonal endothelin antibody(AwETN40) or endothelin A receptor antagonist(FR 139317) failed to attenuate the decline of Cin and histological changes in both right nephrectomized and sham nephrectomized groups. The doses that we used in this experiment was enough to inhibit the hypertensive effects of 1.2 nmol/kg of endothelin. In contrast, the inhibitor of thromboxane A2 synthesis(OKY 046) attenuated the ischemia-induced decreases in urine output, renal blood flow and Cin in sham nephrectomized rats. These results suggest that intrarenal action of thromboxane A2 but not of endothelin may play a key role in right nephrectomy-induced attenuation of ischemic acute renal failure.
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