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大鼠输精管中非肾上腺素能传递的衰竭

Failure of non-adrenergic transmission in the rat vas deferens.

作者信息

Ebong O O, Zar M A

机构信息

Department of Pharmacological Sciences, Medical School, University of Newcastle upon Tyne, U.K.

出版信息

Neuropharmacology. 1989 Apr;28(4):335-41. doi: 10.1016/0028-3908(89)90027-0.

DOI:10.1016/0028-3908(89)90027-0
PMID:2546086
Abstract

Repetitive field stimulation of the vas deferens of the rat with long trains of pulses (90 pulses, 10 Hz, 1 msec) at intervals of 30 or 60 sec produced a decline in the heights of contractile responses. This decline in responses was much more pronounced in phentolamine (5 microM)-treated than in untreated preparations and in the prostatic rather than in the epididymal end of the vas deferens. The decline in the responses was dependent on the number of pulses/train, the frequency of pulses in the train and the interval between successive trains. Potassium chloride (KCl)-induced and adenosine triphosphate (ATP)-induced contractions were largely unaltered after 30 min of stimulation. The decline in the responses was significantly reduced in low but not in high extracellular calcium. 4-Aminopyridine (4-AP) caused an initial potentiation of contractile responses, followed by a faster decline of responses. The decline in responses was more intense in vas deferens from reserpine-treated animals. The results support the view that electrical stimulation-induced decay of motor transmission in the vas deferens of the rat is caused by a specific failure of the non-adrenergic transmission.

摘要

以30或60秒的间隔,用长串脉冲(90个脉冲,10赫兹,1毫秒)对大鼠输精管进行重复场刺激,会导致收缩反应高度下降。与未处理的标本相比,在酚妥拉明(5微摩尔)处理的标本中,这种反应下降更为明显,且在输精管的前列腺端而非附睾端更为明显。反应的下降取决于每串脉冲的数量、串中脉冲的频率以及连续串之间的间隔。刺激30分钟后,氯化钾(KCl)诱导的和三磷酸腺苷(ATP)诱导的收缩基本未改变。在低细胞外钙浓度下,反应的下降显著减少,但在高细胞外钙浓度下则不然。4-氨基吡啶(4-AP)会导致收缩反应最初增强,随后反应下降更快。在利血平处理的动物的输精管中,反应的下降更为强烈。结果支持这样一种观点,即电刺激诱导的大鼠输精管运动传递衰减是由非肾上腺素能传递的特定失败引起的。

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引用本文的文献

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The fade of the purinergic neurogenic contraction of the guinea-pig vas deferens: analysis of possible mechanisms.豚鼠输精管嘌呤能神经源性收缩的消退:可能机制的分析。
Naunyn Schmiedebergs Arch Pharmacol. 1994 Nov;350(5):482-90. doi: 10.1007/BF00173017.