Johnson D G, Ensinck J W
Diabetes. 1976 Aug;25(8):645-9. doi: 10.2337/diab.25.8.645.
Toxin from the scorpion Leiurus quinquestriatus was used to release norepinephrine from sympathetic nerve endings in the perfused rat pancrease. Addition of toxin, 10 mug./ml., to perfusate containing 0.3 mg./ml. glucose caused a large increase in release of norepinephrine and glucagon. Glucagon secretion was suppressed by perfusate containing 3.0 mg./ml. glucose but still responded to stimulation with scorpion toxin. Atropine, 10 muM, had no effect on either norepinephrine or glucagon release in response to scorpion toxin. The release of glucagon was blocked by 100 muM propranolol, 10 muM phentolamine, or 30 muM phenoxybenzamine. Somatostatin, 55nM, did not affect the release of norepinephrine by scorpion toxin but totally inhibited the glucagon response. These results suggest that pharmacologic stimulation of the adrenergic nerve endings in the rat pancreas can elicit a rapid release of glucagon. This response can be prevented by appropriate concentrations of either alpha or beta adrenergic blocking agents or somatostatin.
来自以色列金蝎的毒素被用于从灌注大鼠胰腺的交感神经末梢释放去甲肾上腺素。向含有0.3毫克/毫升葡萄糖的灌注液中添加10微克/毫升的毒素,会导致去甲肾上腺素和胰高血糖素的释放大幅增加。含有3.0毫克/毫升葡萄糖的灌注液会抑制胰高血糖素的分泌,但胰高血糖素仍对蝎毒素刺激有反应。10微摩尔的阿托品对蝎毒素引起的去甲肾上腺素或胰高血糖素释放均无影响。100微摩尔的普萘洛尔、10微摩尔的酚妥拉明或30微摩尔的酚苄明可阻断胰高血糖素的释放。55纳摩尔的生长抑素不影响蝎毒素引起的去甲肾上腺素释放,但完全抑制胰高血糖素反应。这些结果表明,对大鼠胰腺中肾上腺素能神经末梢的药理刺激可引发胰高血糖素的快速释放。适当浓度的α或β肾上腺素能阻断剂或生长抑素可阻止这种反应。