Gutman Y, Boonyaviroj P
Naunyn Schmiedebergs Arch Pharmacol. 1977 Feb;296(3):293-6. doi: 10.1007/BF00498696.
Catecholamine (CA) release was studied in rat adrenal incubated in vitro. Inhibition of (Na + K)-ATPase either by omission of K+ from the incubation medium or by addition of a high concentration of ouabain (10(-3) M) caused increased release of CA from the adrenal. Diphenylhydantoin (DPH) (10(-5) M) inhibited the spontaneous as well as the acetylcholine (10(-4) M)-induced release of CA. However, in K+-free medium or in the presence of 10(-3) M ouabain, DPH had no significant effect on CA release. A low concentration of ouabain (10(-10) M) caused a significant inhibition of spontaneous and of acetylcholine-induced release of CA. In a K+-free medium ouabain (10(-10) M) had no effect on CA release. DPH (10(-5) M) and a low concentration of ouabain (10(-10) M) caused a significant activation of (Na + K)-ATPase in a membrane fraction of the adrenal medulla. It is suggested that DPH and low ouabain concentrations inhibit CA release from the adrenal by activation of the sodium pump. The possible mechanism involved is discussed.
在体外培养的大鼠肾上腺中研究了儿茶酚胺（CA）的释放。通过从培养液中去除钾离子或添加高浓度的哇巴因（10⁻³ M）来抑制（钠 + 钾）-ATP酶，会导致肾上腺中CA释放增加。苯妥英（DPH）（10⁻⁵ M）抑制CA的自发释放以及乙酰胆碱（10⁻⁴ M）诱导的CA释放。然而，在无钾培养基中或存在10⁻³ M哇巴因的情况下，DPH对CA释放没有显著影响。低浓度的哇巴因（10⁻¹⁰ M）可显著抑制CA的自发释放和乙酰胆碱诱导的释放。在无钾培养基中，哇巴因（10⁻¹⁰ M）对CA释放没有影响。DPH（10⁻⁵ M）和低浓度的哇巴因（10⁻¹⁰ M）可显著激活肾上腺髓质膜组分中的（钠 + 钾）-ATP酶。提示DPH和低浓度哇巴因通过激活钠泵来抑制肾上腺中CA的释放。并讨论了其中可能涉及的机制。
