Kaneto A, Kajinuma H, Kosaka K
Horm Metab Res. 1977 Jul;9(4):267-71. doi: 10.1055/s-0028-1093549.
To see the effect of alpha adrenergic receptor stimulation upon in vivo basal secretion of glucagon and insulin, phenylephrine and methoxamine were infused at a dose of 236 pmol/kg/min and 2.36 nmol/kg/min, respectively, for 10 min into the cranial pancreaticoduodenal artery in anesthetized dogs. During the infusion of either drug pancreatic venous blood flow was markedly diminished, resulting in a significant decrease of basal output of both glucagon and insulin. Intrapancreatic administration of the stimulants exerted neglible effects on the plasma levels of both hormones in the systemic circulation. Pretreatment with phentolamine abolished the alpha stimulant-induced inhibition of bihormonal output. Under alpha blockade which per se results effectively in a stimulation of insulin release, basal output of glucagon was not significantly augmented. These results suggest that the alpha receptors on the A cell of the islets may be involved in the similar inhibitor mechanism, but less potently than those on the B cell under basal physiological adrenergic control in the canine.
为观察α肾上腺素能受体刺激对体内胰高血糖素和胰岛素基础分泌的影响,分别以236 pmol/kg/分钟和2.36 nmol/kg/分钟的剂量,向麻醉犬的胰十二指肠上动脉输注去氧肾上腺素和甲氧明10分钟。在输注任何一种药物期间,胰腺静脉血流均显著减少,导致胰高血糖素和胰岛素的基础分泌量显著降低。胰腺内给予刺激剂对全身循环中两种激素的血浆水平影响可忽略不计。酚妥拉明预处理可消除α兴奋剂诱导的双激素分泌抑制。在α受体阻断(其本身可有效刺激胰岛素释放)的情况下,胰高血糖素的基础分泌量并未显著增加。这些结果表明,在犬的基础生理肾上腺素能控制下,胰岛A细胞上的α受体可能参与类似的抑制机制,但作用强度低于B细胞上的α受体。