Elevation in plasma catecholamines in response to insulin stress is under both neuronal and nonneuronal control.
Elevation in plasma catecholamines in response to insulin stress is under both neuronal and nonneuronal control.
复制标题
胰岛素应激引起的血浆儿茶酚胺升高受到神经元和非神经元的控制。
作者：
Zeinab Khalil;Philip D. Marley;B. G. Livett
我们研究了成年大鼠静脉注射胰岛素后，神经源性和非神经源性影响对肾上腺儿茶酚胺（CA）分泌的作用。在对照组大鼠和手术或药物肾上腺去神经或肾上腺切除术后的大鼠中测量血浆CA水平。胰岛素诱导的CA分泌是双相的，与胰岛素剂量成比例。第一阶段为神经源性，导致血浆肾上腺素（A）水平中度升高，去甲肾上腺素（NA）水平变化很小或无变化。这种血浆A的神经源性增加通过部分去神经减少，并通过手术完全肾上腺去神经、肾上腺切除术或给予六甲双铵和阿托品消除。第二阶段发生较晚，并产生了显着增加血浆A和NA。当血浆葡萄糖水平降至75 mg/100 ml以下时，开始该阶段。这种迟发性的A和NA释放并没有被手术或药物肾上腺去神经所改变，表明它是非神经元起源的。然而，肾上腺切除后早期和晚期相均消失，表明肾上腺分泌CA是血浆NA和A水平升高的来源。静脉注射葡萄糖也可消除血浆CA的晚期升高。这些数据表明，负责肾上腺CA的非神经源性分泌的机制，以响应胰岛素应激是敏感的低血糖水平。
We have examined the contribution of neurogenic and nonneurogenic influences to the secretion of adrenal catecholamines (CA) in adult rats after iv administration of insulin. Plasma CA levels were measured in control rats and in rats after surgical or pharmacological adrenal denervation or adrenalectomy. Insulin-induced CA secretion was biphasic and proportional to the insulin dose used. The first phase was neurogenic in origin and produced a moderate increase in plasma adrenaline (A) levels, with little or no change in noradrenaline (NA) levels. This neurogenic increase in plasma A was reduced by partial denervation and abolished by surgical complete adrenal denervation, adrenalectomy, or administration of hexamethonium and atropine. The second phase occurred later and produced a dramatic increase in both plasma A and NA. This phase was initiated when the plasma glucose level fell below 75 mg/100 ml. This late release of A and NA was not altered by surgical or pharmacological adrenal denervation, showing that it was nonneuronal in origin. However, both the early and late phases were abolished by adrenalectomy, showing that adrenal secretion of CA was the origin of the increased plasma levels of NA and A. The late rise in plasma CA was also abolished by iv administration of glucose. These data suggest that the mechanism responsible for the nonneurogenic secretion of adrenal CA in response to insulin stress was sensitive to the level of hypoglycemia.