Sympathetic vasodilatation, kallikrein release and adrenergic receptors in the cat submandibular salivary gland.
Sympathetic vasodilatation, kallikrein release and adrenergic receptors in the cat submandibular salivary gland.
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猫颌下唾液腺中的交感血管舒张、激肽释放酶释放和肾上腺素能受体。
DOI：
10.1111/j.1748-1716.1974.tb05606.x
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发表时间：
1974
期刊：
影响因子：
--
通讯作者：
B. Waaler
中科院分区：
文献类型：
--
作者：
K. Gautvik;M. Kriz;K. Lund;B. Waaler
在猫颌下唾液腺中，肾上腺素能受体参与激肽释放酶的分泌和交感神经刺激后的血管扩张。测定腺体匀浆中激肽释放酶含量、静脉流出量和腺体灌流压。与交感神经刺激和近动脉注射去甲肾上腺素相比，异丙肾上腺素不能引起激肽释放酶的分泌。神经刺激和去甲肾上腺素使腺体中激肽释放酶的数量分别减少了60%和50%。α阻断剂REGTIN®可完全抑制神经刺激诱导的激肽释放酶分泌，而肾上腺素能β阻断剂对酶的分泌无抑制作用。因此，在这个腺体中，激肽释放酶的分泌完全是通过激活肾上腺素能α受体来调节的。
β阻滞剂心得安将神经引起的血管扩张减少了约40%。这种交感血管扩张反应是存在的，但在使用Regitin®预处理后显著降低，Regitin®取消了激肽释放酶的分泌和神经诱导的血管反应的血管收缩阶段。这项研究和早期的一份报告(Gautvik，Kriz和Lund-Larsen 1972 a)表明，腺血管中的β-肾上腺素能受体，以及参与激肽释放酶分泌的α-肾上腺素能受体，在交感神经刺激后观察到的该腺体的血管扩张中发挥作用。
The adrenergic receptors involved in secretion of kallikrein and the vasodilatation occurring subsequent to sympathetic nerve stimulation have been studied in the cat submandibular salivary gland. Measurements were made of kallikrein content in glandular homogenate and of venous outflow and glandular perfusion pressure. Isoprenaline failed to cause secretion of kallikrein in contrast to sympathetic nerve stimulation and close arterial injections of noradrenaline. Nerve stimulation and noradrenaline reduced the amount of kallikrein in the glands by 60 and 50 per cent, respectively. The α-blocking agent Regitin® inhibited completely the secretion of kallikrein induced by nerve stimulation, while adrenergic β-blockade had no inhibitory effect on enzyme secretion. In this gland, therefore, the secretion of kallikrein is mediated entirely through activation of adrenergic α-receptors.
The β-blocking agent propranolol reduced the nerve induced vasodilatation by about 40 per cent. This sympathetic vasodilator response was present, but markedly reduced, after pretreatment with Regitin,® which abolished kallikrein secretion and the vasoconstrictor phase of the nerve-induced vascular response. This study and an earlier report (Gautvik, Kriz and Lund-Larsen 1972 a) suggest that β-adrenergic receptors in the glandular vessels, as well as ®aL-adrenergic receptors involved in the secretion of kallikrein, play a role in the vasodilatation observed in this gland subsequent to sympathetic nerve stimulation.