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離體天竺鼠氣管 cholinergic 及 non-adrenergic non-cholinergic 神經傳遞之鈣離子管道亞型

離體天竺鼠氣管 cholinergic 及 non-adrenergic non-cholinergic 神經傳遞之鈣離子管道亞型.

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離體天竺鼠氣管 cholinergic 及 non-adrenergic non-cholinergic 神經傳遞之鈣離子管道亞型

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  1. 離體天竺鼠氣管 cholinergic 及 non-adrenergic non-cholinergic 神經傳遞之鈣離子管道亞型 • 一﹒離體天竺鼠氣管經由電刺激所引起之膽鹼性收縮 (cholinergic contraction) 及非腎非膽性 (non-adrenergic non-cholinergic) 鬆弛 (NANC relaxation) 藉由具有專一性的鈣離子管道阻斷劑的作用來闡述氣管上調控神經傳遞的鈣離子管道亞型。二﹒離體天竺鼠氣管上,經由低頻率與高頻率電刺激所引起之膽鹼性收縮反應會被 N- 亞型鈣離子管道阻斷劑 ω-conotoxin GVIA 及 ω-conotoxin MVIIA 所抑制; ω-agatoxin IVA (P- 亞型阻斷劑)、ω-conotoxin MVIIC (N-、O-、P- 及 Q- 亞型阻斷劑) 及 nifedipine (L- 亞型阻斷劑) 皆不具作用。 然而,Ni2+ (T- 及 R- 亞型阻斷劑) 會促進 (facilitate) 膽鹼性收縮反應,而且當濃度高於 30 mM 時會產生另一遲來的收縮 (late contraction),此收縮發生率及面積均隨 Ni2+ 濃度的增加而增加,它似乎不是乙醯膽鹼、tachykinins 或其它 polypeptides 所引起。三﹒經由低頻率及高頻率電刺激所產生之非腎非膽性鬆弛反應會被 ω-conotoxin GVIA、ω-conotoxin MVIIA 及 Ni2+ 所抑制; ω-agatoxin IVA、ω-conotoxin MVIIC 及 nifedipine 皆不具作用。四﹒這些結果顯示:離體天竺鼠氣管上,膽鹼性收縮反應是受 N- 亞型鈣離子管道所調控,而非腎非膽性鬆弛反應則是受 N-、T- 及 R- 亞型鈣離子管道所調控。

  2. Calcium channel subtypes for cholinergic and non-adrenergic non-cholinergic neurotransmission in the isolated guinea-pig trachea • 1. The Ca2+ channel subtypes of the neurotransmission of isolated guinea-pig trachea were elucidated by monitoring the effects of specific Ca2+ channel blockers on the cholinergic contraction and non-adrenergic non-cholinergic (NANC)relaxation elicited by electrical field stimulation (EFS).2. In the isolatedguinea-pig trachea, the cholinergic contractile responses to low and high frequency of EFS were inhibited by both N-type calcium channel blockers, ω-conotoxin GVIA and ω-conotoxin MVIIA. ω-Agatoxin IVA (a P-type blocker), ω-conotoxin MVIIC (a N-, O-, P- and Q-type blocker) and nifedipine (a L-type blocker)were ineffective. Whereas, Ni2+ (a T- and R-type blocker), facilitated the cholinergic contraction and produced a late contractile phase when its concentration was higher than 30 mM. The more concentration of Ni2+ increased, the moreincidence and its contractile area of the late contraction occurred. The latecontraction seems not due to the effects of acetylcholine, tachykinins and other polypeptides.3. The NANC relaxant response elicited by low and high frequency of EFS was inhibited by ω-conotoxin GVIA, ω-conotoxin MVIIA and Ni2+. ω-Agatoxin IVA, ω-conotoxin MVIIC and nifedipine were ineffective.4. These results suggested that, in the isolated guinea-pig trachea, the cholinergic contraction is regulated by N-type calcium channel while that of NANC relaxationis controlled by N-, T- and R-type calcium channels.

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