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甘丙肽增强大鼠输精管的电刺激和外源性去甲肾上腺素诱导的收缩。

Galanin potentiates electrical stimulation and exogenous norepinephrine-induced contractions in the rat vas deferens.

作者信息

Ohhashi T, Jacobowitz D M

出版信息

Regul Pept. 1985 Oct;12(2):163-71. doi: 10.1016/0167-0115(85)90197-1.

Abstract

In order to evaluate the mode of action of galanin (GAL) on the neuroeffector mechanism of peripheral sympathetic nerve fibers, the effects of this peptide were tested on the electrical stimulated and the unstimulated preparations of the isolated rat vas deferens in the presence of 10(-7) M atropine. The contractile responses, which were mediated predominantly by activation of postganglionic noradrenergic nerve fibers were dose-dependently potentiated by GAL in concentrations ranging from 1 to 50 nM. The facilitatory action induced by GAL in high concentrations (greater than 10 nM) usually returned to the control level at 2-3 min and were tachyphylactic. The potentiating action of GAL was not modified by pretreatment with 10(-7) M propranolol. Contractions produced by exogenous norepinephrine (NE) in the unstimulated preparations were not affected by pretreatment with low concentrations (less than 5 nM) of GAL. On the other hand, the contractions were dose-dependently potentiated 1 min after pretreatment with higher concentrations (greater than 10 nM) of GAL, which recovered 15 min after constant flow washout. Contractions developed by exogenous 5-hydroxytryptamine were not affected, or slightly inhibited, by GAL (1-50 nM). In some preparations without electrical stimulation, high concentrations of GAL caused a slight contraction, which was not blocked by pretreatment with 10(-6) M phentolamine and 10(-6) M tetrodotoxin. These results suggest that GAL receptors exist presynaptically in the rat vas deferens and that stimulation of the receptors by GAL potentiates the release of NE from the nerve terminals during postganglionic sympathetic nerve stimulation. Other mechanisms for GAL action, such as influence on neuronal uptake and catecholamine metabolism, cannot be ruled out.

摘要

为了评估甘丙肽(GAL)对外周交感神经纤维神经效应机制的作用方式,在10⁻⁷ M阿托品存在的情况下,测试了该肽对分离的大鼠输精管电刺激和未刺激制剂的影响。主要由节后去甲肾上腺素能神经纤维激活介导的收缩反应,在1至50 nM浓度范围内,被GAL剂量依赖性增强。高浓度(大于10 nM)的GAL诱导的促进作用通常在2 - 3分钟时恢复到对照水平,且具有快速耐受性。GAL的增强作用不受10⁻⁷ M普萘洛尔预处理的影响。未刺激制剂中外源性去甲肾上腺素(NE)产生的收缩不受低浓度(小于5 nM)GAL预处理的影响。另一方面,用较高浓度(大于10 nM)的GAL预处理1分钟后,收缩被剂量依赖性增强,在持续冲洗15分钟后恢复。外源性5 - 羟色胺引起的收缩不受GAL(1 - 50 nM)影响或略有抑制。在一些无电刺激的制剂中,高浓度的GAL引起轻微收缩,这种收缩不受10⁻⁶ M酚妥拉明和10⁻⁶ M河豚毒素预处理的阻断。这些结果表明,GAL受体存在于大鼠输精管的突触前,并且在节后交感神经刺激期间,GAL对受体的刺激增强了神经末梢NE的释放。不能排除GAL作用的其他机制,如对神经元摄取和儿茶酚胺代谢的影响。

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