Danielsson A, Sehlin J
Acta Physiol Scand. 1983 Apr;117(4):561-6. doi: 10.1111/j.1748-1716.1983.tb07227.x.
Minute pieces of rat parotid gland were used in studies of adrenergic regulation of K+ efflux using 86Rb+ as a probe for K+. Noradrenaline induced a concentration-dependent RB+ efflux, whereas the beta 1-selective agonist prenalterol was without effect. On the other hand, the beta 2-selective drug, terbutaline, at high concentrations displayed a small enhancement of Rb+-secretion. The selective alpha 1-adrenoceptor drug, phenylephrine, was as potent as noradrenaline, whereas the alpha 2-agonist clonidine had only a small effect. The noradrenaline-induced Rb+-efflux was effectively inhibited in the presence of prazosin, an alpha 1-blocker, whereas the alpha 2-antagonist, yohimbine, was roughly 50 times less potent. The results suggest that catecholamine-induced K+-secretion from the rat parotid gland is mediated via activation of post-synaptic alpha-adrenoceptors of the alpha 1-subtype.
使用86Rb+作为钾离子的探针,将大鼠腮腺的微小组织块用于肾上腺素能对钾离子外流调节的研究。去甲肾上腺素诱导了浓度依赖性的铷离子外流,而β1选择性激动剂普瑞特罗则无作用。另一方面,β2选择性药物特布他林在高浓度时显示出铷离子分泌的轻微增强。选择性α1肾上腺素能受体药物去氧肾上腺素与去甲肾上腺素的效力相当,而α2激动剂可乐定只有轻微作用。在α1阻滞剂哌唑嗪存在的情况下,去甲肾上腺素诱导的铷离子外流被有效抑制,而α2拮抗剂育亨宾的效力约低50倍。结果表明,儿茶酚胺诱导的大鼠腮腺钾离子分泌是通过激活突触后α1亚型的α肾上腺素能受体介导的。