Kudo T, Kotani Y, Oka M, Matsumoto K, Inoki R
Adv Exp Med Biol. 1979;120A:425-37. doi: 10.1007/978-1-4757-0926-1_39.
The effects of the sympathetic nerve stimulation and the administrations of sympathomimetics on the secretion of salivary kallikrein induced by the chorda tympani stimulation were examined quantitatively and qualitatively in the submandibular gland of the dog. The secretion of salivary kallikrein may be mediated through both adrenergic alpha- and beta-receptors. The activities of salivary kallikrein secreted by either the chorda tympani stimulation or isoproterenol were not inhibited by soy bean trypsin inhibitor in vitro, but those secreted by the sympathetic nerve stimulation and noradrenaline or adrenaline were markedly inhibited in vitro. These results suggested that secretion of glandular kallikrein was induced by the chorda tympani stimulation and the sympathetic beta-stimulation, and secretion of plasma kallikrein was induced by the sympathetic alpha-stimulation.
在犬的下颌下腺中,对交感神经刺激以及给予拟交感神经药对鼓索神经刺激诱导的唾液激肽释放酶分泌的影响进行了定量和定性研究。唾液激肽释放酶的分泌可能通过肾上腺素能α受体和β受体介导。鼓索神经刺激或异丙肾上腺素分泌的唾液激肽释放酶的活性在体外不受大豆胰蛋白酶抑制剂的抑制,但交感神经刺激以及去甲肾上腺素或肾上腺素分泌的唾液激肽释放酶的活性在体外受到显著抑制。这些结果表明,腺性激肽释放酶的分泌由鼓索神经刺激和交感β刺激诱导,而血浆激肽释放酶的分泌由交感α刺激诱导。