1988 Fiscal Year Final Research Report Summary
Autoantibody against muscarininc acetylcholine Receptor as a possible cause of Raynauds'phenomenon.
| Project/Area Number |
62570372
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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 |
Neurology
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| Research Institution | Fujita-Gakuen Health University |
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Principal Investigator |
TORIKAI Katsutaka Professor, Dept. of Internal Medicine, School of Medicine., 医学部 内科学, 教授 (50084520)
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| Co-Investigator(Kenkyū-buntansha) |
NAGATA Yutaka Professor, Dept, of Physiology, School of Medicine., 医学部 生理学, 教授 (70084499)
INADA Shinichi Assistant Professor, Dept. of Internal Medicine, School of Medicine., 医学部 内科学, 講師 (70129336)
YOSHIDA Syunji Associate, Dept. of Internal Medicine, School of Medicine., 医学部 内科学, 助手 (00166951)
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| Project Period (FY) |
1987 – 1988
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| Keywords | Raynaud's phenomenon / Collagen Disease / Autoantibody / Arterial Relaxing Faotor / Acetycholine Receptor / 血管内皮 |
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| Research Abstract |
We tried to unlock the mechanism of the occurrence of Raynaud's phenomenon in collagen diseases. Due to the presence of auto-antibodies to muscarinic acetylcholine receptor (m-AchR), hypofunction of m-AchR at the vascular level could occur, and this would be responsible for hindering the inhibition of angiospasm. We therefore studied the possibilities of the development of Raynaud's phenomenon. At the beginning, we determined antibodies using m-AchR extracted from a human brain as an antigen, with the result that we identified a factor inhibiting m-AchR in serum IiG in collagendisease patients with Raynaud's phenomenon. Taking notice of report stating that EDRF (vascular relaxation factor) is secreted from angio-endothelial cells, we also considered the possibilities of a lowering of EDRF levels due to the cytotoxic activity of the patient's serum for endothelial cells. The result was that rate of "dead cells" (this was determined by the dye exclusion method), which was used to indicate the impeding activity of the patient's whole serum for endothelial cells, was significantly higher in both Raynaud's phenomenon positivity and vasculitis complication groups than in healthy volunteers as controls. The patient's serum gamma-globulin and IgG fractions were then purified and examined, with the result that the rate of "dead cells" was higher in the Raynaud's phenomenen positivity group than in the control group. These results suggested that the development of Raynaud's symptoms may be associated not only with auto-antibodies to m-AchR but also with impediment of EDRF which is reportedly secreted from vascular endothelial cells.
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