| Project/Area Number |
12670099
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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 |
General pharmacology
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| Research Institution | Mukogawa Women's University |
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Principal Investigator |
SHINOZUKA Kazumasa Mukogawa Women's University, Faculty of Pharmaceutical sciences, Professor, 薬学部, 教授 (50117777)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 2001: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2000: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | noradrenaline / rat prostate / purinoceptor / ATP / α receptor / adrenergic nerve terminal / electric stimulation / 交感神経 / ノルアドレナリン遊離 / シナプス前受容体 |
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| Research Abstract |
In this study, the effects of purinoceptor agonists on the release of endogenous noradrenaline (NA) evoked electrical field stimulation (EPS) prostate gland of the rat were examined. NA was quantified by HPLC coupled with electrochemical detection techniques. 1) There are two kind of purinoceptors (PI and P?) inhibiting NA-release on adrenergic nerve terminals in rat prostate. 2) NA evoked by high-frequency EPS (8 Hz) induces purines-release via a, receptor on effector cells. The amount of purines-release evoked by EPS was higher than that of NA-release (total purines : NA= 100 : 1). 3) Purines evoked by stimulation of a, receptor on effector cells affect prejunctional purinoceptor (PI and P?), and inhibit NA-release. 4) Inhibition of NA-release via prejunctional purinoceptors consequently induces the decreases of the tone in prostate smooth muscle. 5) These results indicate that excess NA evoked by high frequency EPS induced abundant purines-release from effector cells with excess contraction, and consequently inhibit NA- release and decrease the tone of contraction.
The adrenergic nerve plays an important role in the control of prostate smooth muscle tone. It is well known that NA-release is regulated by feedback inhibition through prejunctional a2-adrenoceptors in most tissues. However, very few attempts have been made to investigate the regulation of neurotransmission through prejunctional purinoceptors in the prostate. In this investigation, we suggested the existence of transsynaptic neuromodulation by purines derived from effector cells.
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