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哇巴因对离体豚鼠输精管外周肾上腺素能神经元去甲肾上腺素释放的影响。

The effect of ouabain on noradrenaline output from peripheral adrenergic neurones of isolated guinea-pig vas deferens.

作者信息

Nakazato Y, Ohga A, Onoda Y

出版信息

J Physiol. 1978 May;278:45-54. doi: 10.1113/jphysiol.1978.sp012291.

Abstract
  1. The effect of ouabain on the noradrenaline output from peripheral adrenergic neurones has been studied using isolated guinea-pig vasa deferentia.2. Exposure to ouabain (10(-4)M) causes a gradual increase in the noradrenaline output. The effect occurs after a delay of 20 min and reaches a maximum during the period from 40-60 min.3. In the absence of external Ca, exposure to ouabain fails to produce an increase in the noradrenaline output. However, the reintroduction of Ca (2.5 mM) after a 1 hr exposure to ouabain in Ca-free media causes a rapid rise in noradrenaline output which reaches a maximum within the first 20 min.4. After a 1 hr exposure to a low concentration of ouabain (10(-5)M) the reintroduction of Ca is almost ineffective in increasing the noradrenaline output. When the concentration of ouabain is increased, the reintroduction of Ca becomes effective and causes a maximum effect with 10(-4)M ouabain. In the presence of a constant amount of ouabain (10(-4)M) the noradrenaline output induced by the reintroduction of Ca increases over the range 0.2-2.5 mM.5. In the presence of ouabain (10(-4)M) the Ca-induced noradrenaline output increases in a linear fashion with increasing Na concentrations from 25 to 143 mM, as long as NaCl is replaced with equimolar choline chloride or isotonic sucrose.6. In the presence of the lowest effective concentration of sodium (25 mM) the noradrenaline output induced by the reintroduction of Ca after a 1 hr exposure to ouabain is potentiated by LiCl. However, in the complete absence of Na(+) ions, there is no Li-dependent increase in the Ca-induced noradrenaline output.7. It is suggested that ouabain may cause an increase in noradrenaline output by an effect on the Na-dependent Ca influx system.
摘要
  1. 利用离体豚鼠输精管研究了哇巴因对外周肾上腺素能神经元去甲肾上腺素释放量的影响。

  2. 暴露于哇巴因(10⁻⁴M)会导致去甲肾上腺素释放量逐渐增加。该效应在延迟20分钟后出现,并在40 - 60分钟期间达到最大值。

  3. 在无细胞外钙的情况下,暴露于哇巴因不会使去甲肾上腺素释放量增加。然而,在无钙培养基中暴露于哇巴因1小时后重新加入钙(2.5 mM)会导致去甲肾上腺素释放量迅速增加,并在最初20分钟内达到最大值。

  4. 在暴露于低浓度哇巴因(10⁻⁵M)1小时后,重新加入钙对增加去甲肾上腺素释放量几乎无效。当哇巴因浓度增加时,重新加入钙变得有效,并在10⁻⁴M哇巴因时产生最大效应。在存在恒定剂量的哇巴因(10⁻⁴M)时,重新加入钙诱导的去甲肾上腺素释放在0.2 - 2.5 mM范围内增加。

  5. 在存在哇巴因(10⁻⁴M)的情况下,只要用等摩尔的氯化胆碱或等渗蔗糖替代氯化钠,随着钠浓度从25 mM增加到143 mM,钙诱导的去甲肾上腺素释放量呈线性增加。

  6. 在存在最低有效浓度的钠(25 mM)时,在暴露于哇巴因1小时后重新加入钙诱导的去甲肾上腺素释放量会被氯化锂增强。然而,在完全不存在钠离子的情况下,钙诱导的去甲肾上腺素释放量没有锂依赖性增加。

  7. 有人提出,哇巴因可能通过影响钠依赖性钙内流系统导致去甲肾上腺素释放量增加。

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