Imura H, Kato Y, Ikeda M, Morimoto M, Yawata M
J Clin Invest. 1971 May;50(5):1069-79. doi: 10.1172/JCI106578.
In order to determine whether an adrenergic mechanism is involved in the secretion of growth hormone and insulin, the effect of adrenergic-blocking or -stimulating agents on plasma human growth hormone (HGH), immunoreactive insulin, blood free fatty acids (FFA), and glucose levels was studied in normal human subjects. The intravenous infusion of propranolol, a beta adrenergic-blocking agent, caused a rise in plasma HGH, a transient decrease in blood FFA, and no significant change in plasma insulin. This increase in plasma HGH was inhibited either by the combined administration of isoproterenol, a beta adrenergic-stimulating agent, along with propranolol or by oral glucose loading immediately before the start of propranolol infusion. The concomitant administration of epinephrine and propranolol brought about a rise in plasma HGH comparable with that produced by propranolol alone, without any significant change in blood FFA. Alpha adrenergic blockade by the intravenous infusion of phenotolamine significantly suppressed plasma HGH responses to insulin-induced hypoglycemia and to arginine infusion, and enhanced plasma insulin response to arginine infusion. It also stimulated lipid mobilization significantly. The intravenous infusion of alpha adrenergic-stimulating agents, phenylephrine and methoxamine, caused an increase in plasma HGH, a slight decrease in blood FFA, and no significant change in plasma insulin. This increase in plasma HGH was significantly inhibited by the simultaneous administration of phentolamine along with methoxamine. On the contrary, a beta adrenergic stimulant, isoproterenol, raised plasma insulin and blood FFA, and abolished the plasma HGH response to propranolol. Another beta stimulator, isoxsuprine, raised blood FFA but not plasma insulin. It is concluded that either beta adrenergic blockade or alpha stimulation enhances HGH secretion and inhibits insulin secretion and fat mobilization, whereas either alpha blockade or beta stimulation stimulates insulin secretion and fat mobilization and inhibits HGH secretion.
为了确定肾上腺素能机制是否参与生长激素和胰岛素的分泌，研究了肾上腺素能阻断剂或激动剂对正常人体血浆人生长激素（HGH）、免疫反应性胰岛素、血游离脂肪酸（FFA）和葡萄糖水平的影响。静脉输注β肾上腺素能阻断剂普萘洛尔导致血浆HGH升高、血FFA短暂降低，而血浆胰岛素无显著变化。血浆HGH的这种升高可被β肾上腺素能激动剂异丙肾上腺素与普萘洛尔联合给药或在普萘洛尔输注开始前立即口服葡萄糖负荷所抑制。肾上腺素与普萘洛尔同时给药使血浆HGH升高，与单独使用普萘洛尔产生的升高相当，而血FFA无任何显著变化。静脉输注酚妥拉明进行α肾上腺素能阻断可显著抑制血浆HGH对胰岛素诱导的低血糖和精氨酸输注的反应，并增强血浆胰岛素对精氨酸输注的反应。它还显著刺激脂质动员。静脉输注α肾上腺素能激动剂去氧肾上腺素和甲氧明导致血浆HGH升高、血FFA略有降低，而血浆胰岛素无显著变化。血浆HGH的这种升高可被酚妥拉明与甲氧明同时给药显著抑制。相反，β肾上腺素能激动剂异丙肾上腺素使血浆胰岛素和血FFA升高，并消除了血浆HGH对普萘洛尔的反应。另一种β激动剂异舒普林使血FFA升高，但不使血浆胰岛素升高。结论是，β肾上腺素能阻断或α刺激均可增强HGH分泌并抑制胰岛素分泌和脂肪动员，而α阻断或β刺激则刺激胰岛素分泌和脂肪动员并抑制HGH分泌。
