Smith P A, Dombro K R
Can J Physiol Pharmacol. 1985 Sep;63(9):1182-9. doi: 10.1139/y85-194.
Two different electrophysiological responses in amphibian sympathetic ganglia were studied by means of the sucrose gap technique; the potassium-activated hyperpolarization (KH) which serves as an index of electrogenic Na+ pumping, and the hyperpolarization induced by adrenaline (AdH). Under appropriate experimental conditions, 0.1 microM adrenaline potentiated the KH to 121.5 +/- 7.5% of control (n = 7). This potentiation was blocked by both yohimbine (50 nM) and prazosin (1 microM) but not by propranolol (1 microM). Clonidine (10 nM) potentiated the KH to 113.5 +/- 3.4% of control (n = 5), whereas methoxamine (0.1 microM) was ineffective. Several lines of evidence argued against the hypothesis that the AdH may be generated, in whole or in part, by stimulation of the Na+ pump. For example, the AdH was sometimes completely unaffected when the KH was blocked by ouabain, and the AdH was eliminated by 2 mM Ba2+ even though this cation enhanced membrane hyperpolarization accompanying electrogenic Na+ pumping. These results imply that the electrogenic Na+ pump is not involved in the short-term electrophysiological effects of catecholamines. Despite this, it is possible that the homeostasis of Na+ and K+ in nerve may be regulated by alpha-adrenergic mechanisms.
利用蔗糖间隙技术研究了两栖类交感神经节中的两种不同电生理反应；钾激活超极化（KH）作为电生钠泵的指标，以及肾上腺素诱导的超极化（AdH）。在适当的实验条件下，0.1微摩尔肾上腺素将KH增强至对照的121.5±7.5%（n = 7）。这种增强作用被育亨宾（50纳摩尔）和哌唑嗪（1微摩尔）阻断，但不被普萘洛尔（1微摩尔）阻断。可乐定（10纳摩尔）将KH增强至对照的113.5±3.4%（n = 5），而甲氧明（0.1微摩尔）无效。几条证据反驳了AdH可能全部或部分由钠泵刺激产生的假说。例如，当KH被哇巴因阻断时，AdH有时完全不受影响，并且AdH被2毫摩尔钡离子消除，尽管这种阳离子增强了伴随电生钠泵的膜超极化。这些结果表明电生钠泵不参与儿茶酚胺的短期电生理效应。尽管如此，神经中钠和钾的稳态仍有可能受α-肾上腺素能机制调节。
