Arbilla S, Langer S Z
Br J Pharmacol. 1978 Oct;64(2):259-64. doi: 10.1111/j.1476-5381.1978.tb17298.x.
The alpha-adrenoceptor blocking agent, tolazoline, and the O-methylated metabolite of adrenaline, metanephrine, produced a concentration-dependent increase of tension in the smooth muscle of the cat isolated nictitating membrane. These effects were considered to be due to the activation of postsynaptic alpha-adrenoceptors. 2 The responses to nerve stimulation of this muscle were neither potentiated nor blocked by tolazoline (0.1 to 10 micrometer) or metanephrine (1 to 10 micrometer). 3 3H-transmitter overflow evoked by electrical stimulation was not modified by tolazoline or metanephrine in concentrations in which these drugs stimulated the postsynaptic alpha-adrenoceptors. 4 Since tolazoline and metanephrine failed to activate the presynaptic alpha-adrenoceptors of the cat nictitating membrane under experimental conditions in which they stimulated the postsynaptic alpha-adrenoceptors, these results further support the view that the presynaptic (alpha2) adrenoceptors differ from the postsynaptic (alpha1) adrenoceptors.
α-肾上腺素受体阻断剂妥拉唑啉和肾上腺素的O-甲基化代谢产物间甲肾上腺素,可使猫离体瞬膜平滑肌的张力呈浓度依赖性增加。这些效应被认为是由于突触后α-肾上腺素受体的激活所致。2 妥拉唑啉(0.1至10微摩尔)或间甲肾上腺素(1至10微摩尔)对该肌肉神经刺激的反应既无增强也无阻断作用。3 电刺激诱发的3H递质溢出未被能刺激突触后α-肾上腺素受体的浓度的妥拉唑啉或间甲肾上腺素所改变。4 由于在刺激突触后α-肾上腺素受体的实验条件下,妥拉唑啉和间甲肾上腺素未能激活猫瞬膜的突触前α-肾上腺素受体,这些结果进一步支持了突触前(α2)肾上腺素受体与突触后(α1)肾上腺素受体不同的观点。