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| 發表人 | 討論主題 | 發表時間 | 討論數 |
| 蒙恩 | 乙醯膽鹼和蕈毒受體在膀胱輸入神經活動的抑制角色 | 2010/7/28 下午 05:08:47 | 0 |
| 原 文 | 題 目 | The Inhibitory Role of Acetylcholine and Muscarinic Receptors in Bladder Afferent Activity |
| 作 者 | Daly DM, Chess-Williams R, Chapple C & Grundy D. | |
| 出 處 | J Urol. 2010;58(1):22-28 | |
| 出版日期 | Jul, 2010 | |
| 評 論 |
乙醯膽鹼拮抗劑是目前治療膀胱過動症的主要藥物。原本大家都認為此種藥物是靠著抑制副交感神經末梢釋放的乙醯膽鹼(acetylcholine)作用在膀胱逼尿肌上，以達到治療效果。近年來急尿感和頻尿症狀都被認為和輸入神經(afferent nerve)的異常傳導有密切的關係，而且最近有愈來愈多證據顯示，乙醯膽鹼拮抗劑可能也會影響輸入神經的活動，所以作者們利用帶有輸入神經的小鼠膀胱來試驗乙醯膽鹼和蕈毒受體如何影響輸入神經的活動。 阿托品（Atropine）為一種乙醯膽鹼拮抗劑(acetylcholine antagonist, antacholinergic)，可逆地阻礙乙醯膽鹼與蕈毒鹼受體(Muscarinic receptor)之結合。作者在給予阿托品後，並不影響自發性的輸入神經活動、膀胱脹大後輸入神經的反應或膀胱順應性。但在給予乙醯膽鹼促效藥(如Bethanechol, Carbachol…)刺激蕈毒鹼受體後，竟發現自發性的輸入神經活動被抑制，且膀胱順應性明顯降低。若是事先加入鈣離子拮抗劑 (硝苯地平; Nifedipine)抑制膀胱張力，再加入乙醯膽鹼促效藥，自發性輸入神經活動及膀胱順應性降低的情況依舊存在。根據這個實驗的結果，作者認為蕈毒鹼受體在受到刺激後會抑制輸入神經的活動，且此種抑制效應與膀胱張力無關。總結來說，乙醯膽鹼的神經傳導與正常或是發生病變的膀胱輸入神經活動有一定的關聯。這篇文章幫助科學家們對膀胱過動症病因和治療機轉有更進一步的了解。 |
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| abstract | BACKGROUND: The main treatment for overactive bladder (OAB) is the use of anticholinergic drugs initially believed to inhibit the effect of parasympathetic acetylcholine (ACh) on the detrusor; however, there is now evidence to suggest that anticholinergic drugs could interact with sensory pathways. OBJECTIVE: Investigate the role of muscarinic receptors and ACh in modulating bladder afferent sensitivity in the mouse. DESIGN, SETTING, AND PARTICIPANTS: Bladder and surrounding tissue were removed from wild-type male mice, placed in a recording chamber, and continually perfused with fresh oxygenated Krebs solution at 35 degrees C. Bladders were cannulated to allow infusion and intravesical pressure monitoring, and afferent nerve fibres innervating the bladder were dissected and put into a suction electrode for recording. MEASUREMENTS: Multiunit afferent activity and intravesical pressure were recorded at baseline and during bladder distension. Experiments were conducted in the presence of muscarinic agonists and antagonist or in the presence of the cholinesterase inhibitor physostigmine. RESULTS AND LIMITATIONS: Blocking muscarinic receptors using atropine (1muM) had no effect on spontaneous afferent discharge, the afferent response to bladder distension, or on bladder compliance. However, stimulation of muscarinic receptors directly using bethanechol (100muM) and carbachol (100muM) or indirectly using physostigmine (10muM) significantly inhibited the afferent response to bladder distension and concurrently reduced bladder compliance. Furthermore, prior application of nifedipine prevented the changes in bladder tone but did not prevent the attenuation of afferent responses by bethanechol or physostigmine. CONCLUSIONS: These data indicate that stimulation of muscarinic receptor pathways can depress sensory transduction by a mechanism independent of changes in bladder tone, suggesting that muscarinic receptor pathways and ACh could contribute to normal or pathologic bladder sensation. | |
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