1997 Fiscal Year Final Research Report Summary
Molecular basis for occurence of the spontaneous activity of smooth muscle-consisting organs, and its functinal disorder.
| Project/Area Number |
08307020
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
応用薬理学・医療系薬学
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| Research Institution | Kumamoto University |
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Principal Investigator |
NISHI Katsuhide Kumamoto University, School of Medicine, Professor, 医学部, 教授 (00040220)
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| Co-Investigator(Kenkyū-buntansha) |
FUJINO Masayuki Yamanashi Medical College, Dpt.of Internal Medicine, Professor, 教授 (60090487)
ITOH Takeo Nagoya City University, School of Medicine, Professor, 医学部, 教授 (70159888)
ITOH Katsuaki Miyazaki University, Faculty of Agriculture, Professor, 農学部, 教授 (70136795)
ITOH Yuushi Kyusyu University, School of Medicine, Professor, 医学部, 教授 (80037506)
TORIHASHI Shigeko Nagoya University, School of Medicine, Assistant, 医学部, 助手 (90112961)
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| Project Period (FY) |
1996 – 1997
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| Keywords | neutralizing mouse anti-c-Kit antibody / isolated gastric smooth muscle cell / sarcoplasmic reticulum / distribution of c-Kit expressing cells / Cajar's interstitial cell / colon of Hierschprung's disease patient / hunger contraction of the ileum / apamins-sensitive channel |
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| Research Abstract |
Nishi and his co-workers, using mouse-small intestine treated with neutralizing mouse anti-c-Kit antibody (ACK2), examined an intracellular Ca^<2+> handling mechanism in the isolated intestinal smooth muscle, and found that caffeine-induced I_<K.Caf>), carbachol-induced calcium dependent K current (I_<K.Cab>) in isolated intestinal smooth muscle cells treated with ACK2 showed altered characteristics, compared with those in the control ones, suggesting dysfunction of uptake of Ca^<2+> into the calcium storing sites Torihashi examined distribution of c-Kit expressing cells in the human intestine, their ultra structure and relation to the Cajar's interstitial cells, and found a decrease in the number of c-Kit expressing cells in the colon taken from Hirschprung's disease patients. Using ACK2 in the mouse intestine, c-Kit expressing cells were classified into groups of 1)cells not affected by treatment with ACK2, 2)cells showed developmental delay with ACK2 and 3)types of c-Kit expressing
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cells later transfomed into smooth muscle cells Katsuaki Ito examined the distribution of c-Kit expressing cells in the mouse stomach, and found that in the stomach, c-Kit expressing cells had already developed before birth, but not in the c-Kit deficient mutant mouse. Fujino et al, treated mouse with ACK2 and found that c-Kit expressing cell-deficient intestine lacking the regular pacemaker activity, showed abnormal hunger-contraction wave of the intestinal movement, suggesting dysfunction of synchronizing mechanisms of peristaltic in the intestine without pace-maker activity. Ozaki et al showed deficiency of intestinal intermuscular neural ganglia in the caudal part of the intestine in the enodotherin B receptor-deficient mutant mouse, in which hypertrophy of intestinal smooth muscle and decreased spontaneous movements of the intestine cranial to the region without the neural ganglia were observed. Yushi Ito et al examined mechanisms underlying propagating spontaneouslu occurring peristaltic in the ileum by motirin, and found that an increase in activity of calcium currents mediated through anion channels activated by a low concentration of motirin and a marked increase of anion channel activity mediated through muscarinic receptors. Takeo Ito showed that NO exerted negative control on agents-induced contraction in the rabbit cerebral median artery and the arterial smooth muscle was hyperpolarized by activation of apamin-sensitive potassium channels via an increased release of DHF induced by acetylcholine. Takahama examined afferent neural activity related to an increase of tracheal smooth muscle tone and showed that bradykinin affected afferent nerve activity and the effect was also modified by tachkinin. Less
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