Katsuragi T, Usune S, Furukawa T
Eur J Pharmacol. 1982 Jul 9;81(2):217-25. doi: 10.1016/0014-2999(82)90439-3.
The effects of K+-free medium, ouabain or high KCl on the contractile response and spontaneous efflux of adrenaline were analyzed in denervated guinea-pig or rat vasa deferentia preloaded with 3 x 10(-5) M (+/-)-adrenaline. The K+-free medium-induced contraction of guinea-pig tissues was related to the concentration of adrenaline used during preloading and was suppressed by the addition of 2.5 mM Rb+ but not by 2.5 mM Cs+. The contractile effects of K+-free medium and 10(-5) M ouabain, but not the response to high KCl, were prevented by 5 x 10(-6) M phentolamine or 3 x 10(-5) M deoxycorticosterone. These contractions, therefore, appear to be mediated by adrenaline released from the extraneuronal compartment. The K+-free medium- or ouabain-induced contractions of denervated rat vasa deferentia were small in comparison with those of the guinea-pig tissue. The amount of spontaneous efflux of adrenaline from the guinea-pig preparation was significantly enhanced by omission of K+ or by 10(-4) M ouabain but not by 80 mM KCl. K+-free medium and 3 x 10(-5) M ouabain merely elicited a small membrane depolarization accompanied by a slight decrease of membrane resistance in the guinea-pig vas deferens, whereas 30 mM KCl markedly altered these electrical parameters. From these findings, it is suggested that the rapid increase in extraneuronal amine release following inhibition of Na+-K+-ATPase may be due to some direct effect of K+ deficiency or of ouabain on the binding between the enzyme and the catecholamine rather than to alterations of membrane properties as a consequence of enzyme inhibition.
在预先加载3×10⁻⁵ M（±）-肾上腺素的去神经支配的豚鼠或大鼠输精管中，分析了无钾培养基、哇巴因或高浓度氯化钾对收缩反应和肾上腺素自发流出的影响。无钾培养基诱导的豚鼠组织收缩与预加载期间使用的肾上腺素浓度有关，并且添加2.5 mM铷⁺可抑制该收缩，但添加2.5 mM铯⁺则不能。5×10⁻⁶ M酚妥拉明或3×10⁻⁵ M脱氧皮质酮可阻止无钾培养基和10⁻⁵ M哇巴因的收缩作用，但不能阻止对高浓度氯化钾的反应。因此，这些收缩似乎是由神经外间隙释放的肾上腺素介导的。与豚鼠组织相比，去神经支配的大鼠输精管中无钾培养基或哇巴因诱导的收缩较小。豚鼠制剂中肾上腺素的自发流出量通过去除钾⁺或10⁻⁴ M哇巴因而显著增加，但80 mM氯化钾则不能。无钾培养基和3×10⁻⁵ M哇巴因仅在豚鼠输精管中引起轻微的膜去极化，并伴有膜电阻的轻微降低，而30 mM氯化钾则显著改变这些电参数。从这些发现表明，抑制钠钾ATP酶后神经外胺释放的快速增加可能是由于钾⁺缺乏或哇巴因对该酶与儿茶酚胺之间结合的某些直接作用，而不是由于酶抑制导致的膜特性改变。
