Regulation of Salivary Kallikrein Secretion in the Rat Submandibular Gland
Regulation of Salivary Kallikrein Secretion in the Rat Submandibular Gland
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大鼠颌下腺唾液激肽释放酶分泌的调节
DOI：
10.1111/j.1748-1716.1977.tb05919.x
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发表时间：
1977
期刊：
影响因子：
--
通讯作者：
K. Gautvik
中科院分区：
文献类型：
--
作者：
T. Orstavik;K. Gautvik
用bz - arg - oet -酯酶测定各组大鼠颌下腺的湿重、总蛋白含量和激肽激酶活性，并测定激肽激酶抗原活性。研究发现，同一动物的成对腺体具有可比性，而不同动物之间的差异则相当大。两个配对的腺体中的一个被切除并用作对照，另一个随后受到刺激。模拟副交感神经分泌（腹腔注射匹罗卡品；乙酰胆碱灌注并电刺激腺体门附近的导管神经丛）或模拟交感神经（加或不加α或β-肾上腺素阻滞剂刺激颈交感神经；灌注肾上腺素、去甲肾上腺素或异丙肾上腺素）诱导唾液分泌。通过测量腺体总钾化酶含量的变化和唾液中钾化酶的定量来研究其作用。总能观察到少量钾激肽的分泌。然而，oc-肾上腺素能刺激在释放钾激肽方面的效果分别是β-肾上腺素能刺激和副交感神经刺激的40倍和1500倍。此外，β-肾上腺素能刺激比拟副交感神经刺激释放更多的钾化肽。免疫组织化学证实了α-肾上腺素能刺激后小钾化因子的减少。受刺激腺体中钾激肽定位未见改变。
Unstimulated pairs of rat submandibular glands were compared with regard to their wet weight, total protein content and kallikrein activity quantitated by Bz-Arg-OEt-esterase and kallikrein antigenic activity. Paired glands from the same animal were found to be comparable, whereas differences from one animal to another were considerable. One of two paired glands was extirpated and used as control, and the other was subsequently subjected to stimulation. Salivary secretion was induced parasympathomimetically (intraperitoneal injections of pilocarpine; perfusion with acetylcholine and electrical stimulation of the ductal nerve plexus near the gland hilus) or sympathomimetically (cervical sympathetic nerve stimulation with or without administration of α or β-adrenergic blocker; perfusion with epinephrine, norepinephrine or isoproterenol). The effect was studied by measuring the change in total gland kallikrein content and by quantitation of kallikrein in saliva. A small secretion of kallikrein was always observed. However, oc-adrenergic stimulation was 40 and 1500 fold more effective in releasing kallikrein than β-adrenergic and parasympathomimetic stimulation, respectively. Also, significantly more kallikrein was released by β-adrenergic than parasympathomimetic stimulation. Immunohistochemistry confirmed the observed depletion of kallikrein following α-adrenergic stimulation. No alteration in kallikrein localization was observed in stimulated glands.