Röckel A, Preissler A, Heidland A
Adv Exp Med Biol. 1986;198 Pt A:273-7. doi: 10.1007/978-1-4684-5143-6_37.
The effects of pharmacologically induced alterations of alpha 1, alpha 2 and beta-adrenergic system on kallikrein secretion - measured as amidolytic activity - in rat parotid gland were tested in vivo. Beta and alpha 1/2-adrenergic stimulation (Orciprenaline, alpha-methylnorepinephrine) caused a comparably significant increase of parotid kallikrein secretion. Alpha 2-receptor blockade (yohimbine) but not the alpha 1-antagonist prazosin, partly abolished the effect of alpha-methylnorepinephrine. The effects of the alpha 1-adreno-receptor agonist norfenephrine on kallikrein secretion were significantly lower compared to alpha 1/2-adreno-receptor-stimulation.
在体内测试了药理学诱导的α1、α2和β-肾上腺素能系统改变对大鼠腮腺激肽释放酶分泌(以酰胺水解活性衡量)的影响。β和α1/2-肾上腺素能刺激(奥西那林、α-甲基去甲肾上腺素)导致腮腺激肽释放酶分泌出现相当显著的增加。α2-受体阻断剂(育亨宾)而非α1-拮抗剂哌唑嗪部分消除了α-甲基去甲肾上腺素的作用。与α1/2-肾上腺素能刺激相比,α1-肾上腺素能受体激动剂去甲伪麻黄碱对激肽释放酶分泌的影响显著更低。