1996 Fiscal Year Final Research Report Summary
Pressure contributes to mesangial injury associated with sytokines
| Project/Area Number |
07457243
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 | Saitama Medical School |
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Principal Investigator |
SUZUKI Hiromichi Saitama Medical School, Department of Nephrology, Professor, 医学部, 教授 (80129494)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAMOTO Hidetomo Saitama Medical School, Department of Nephrology, Associate, 医学部, 講師 (90180421)
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| Project Period (FY) |
1995 – 1996
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| Keywords | PRESSURE / MESANGIAL CELLS / NEPHROSCLEROSIS / CYTOKINES / ADHESION MOLECULES / APOTOSIS / RENAL ARTERY |
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| Research Abstract |
In clinical study, hypertension has a considerable effect on the renal sclerosis in patients with uninephrectomy more than 20 years ago. Using the isolated perfused hydronephrotic kidney models, nitric oxide modulates myogenic vasoconstriction of the afferent arteriole in spontaneously hypertensive rats, and chloride channels play an important role in afferent arterioleae constriction. In human mesangial cells, angiotensin II was expected to produce collagen synthesis under high pressure, however, no increases in collagen synthesis were found. By contrast, interleukin-4 modulates collagen synthesis. In addition, pressure induced apoptosis. Further, adhesion molecular contribute to apoptosis under high pressure. From these findings, it is suggested that pressure collaborates with cytokines but not angiotensin II and adhesion molecular may induce cytokine production.
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