Skikama H, Ui M
Am J Physiol. 1975 Oct;229(4):962-6. doi: 10.1152/ajplegacy.1975.229.4.962.
Intravenous glucose tolerance in fasting rats was improved by phentolamine, an alpha-adrenergic blocking agent, and diminished by propranolol, a beta-adrenergic blocking agent. These effects of adrenergic blockers were dependent on the action of insulin, secretion of which is controlled by an adrenergic mechanism. Epinephrine caused by hyperglycemia and impaired glucose tolerance. Both actions of epinephrine were partly inhibited by either an alpha or beta blocker and completely abolished by combination of both blockers in normal rats. However, in rats treated with anti-insulin serum or 5-methoxyindole-2-carboxylic acid, a potent inhibitor of gluconeogenesis, both actions of epinephrine were blocked by propranolol alone, but not by phentolamine. It is concluded that beta-receptor-mediated inhibiton of peripheral glucose utilization is primarily responsible for epinephrine-induced hyperglycemia and impairment of glucose tolerance. Furthermore, the reduction of glycemic action of epinephrine observed after alpha blockade is due to the hypoglycemic action of insulin secreted by the stimulation of beta receptors in pancreatic beta cells.
α-肾上腺素能阻滞剂酚妥拉明可改善禁食大鼠的静脉葡萄糖耐量，而β-肾上腺素能阻滞剂普萘洛尔则会降低其静脉葡萄糖耐量。肾上腺素能阻滞剂的这些作用取决于胰岛素的作用，胰岛素的分泌受肾上腺素能机制控制。肾上腺素会导致血糖升高和葡萄糖耐量受损。在正常大鼠中，肾上腺素的这两种作用部分被α或β阻滞剂抑制，而两种阻滞剂联合使用则可完全消除其作用。然而，在用抗胰岛素血清或5-甲氧基吲哚-2-羧酸（一种有效的糖异生抑制剂）处理的大鼠中，肾上腺素的两种作用仅被普萘洛尔阻断，而不被酚妥拉明阻断。得出的结论是，β受体介导的外周葡萄糖利用抑制主要是肾上腺素诱导的高血糖和葡萄糖耐量受损的原因。此外，α受体阻断后观察到的肾上腺素降糖作用的降低是由于胰腺β细胞中β受体受刺激分泌的胰岛素的降糖作用。
