Foster R W, Shah D S, Small R C
Br J Pharmacol. 1978 Feb;62(2):307-13. doi: 10.1111/j.1476-5381.1978.tb08461.x.
Guanethidine, acting on the rat isolated anococcygeus, causes adrenergic neurone blockade (slowly terminated by washing), noradrenaline potentiation and, with higher concentrations, spasm (both rapidly terminated by washing). 2 The spasm is an indirect sympathomimetic action, for it is sensitive to phentolamine and reserpine and shows tachyphylaxis. 3 The concentration of cocaine equieffective with the spasmogenic concentration of guanethidine as an inhibitor of noradrenaline uptake caused much less spasm. Moreover, it did not enhance noradrenaline efflux from anococcygeus loaded with (-)-[3H]-noradrenaline, as guanethidine did. 4 The spasm induced by guanethidine in excess of cocaine is due to guanethidine-evoked noradrenaline release.
胍乙啶作用于大鼠离体尾骨肌时，可引起肾上腺素能神经元阻滞（通过冲洗可缓慢消除）、去甲肾上腺素增强，且在较高浓度时会引起痉挛（两者通过冲洗均可迅速消除）。2 这种痉挛是一种间接拟交感神经作用，因为它对酚妥拉明和利血平敏感且有快速耐受性。3 与胍乙啶致痉挛浓度等效的可卡因浓度作为去甲肾上腺素摄取抑制剂所引起的痉挛要少得多。此外，它不像胍乙啶那样能增强用（-）-[3H]-去甲肾上腺素加载的尾骨肌的去甲肾上腺素外流。4 胍乙啶超过可卡因诱导的痉挛是由于胍乙啶诱发的去甲肾上腺素释放。
