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大量实验证明,肾上腺素能神经-效应器接点突触前膜和突触后膜上的α-受体性质不同,Langers首先提出,将调节效应器官反应的突触后α-受体命名为α_1-受体,而将突触前膜上调节NA释放的α-受体命名为α_2-受体。一些药物可选择性地激动或阻断突触前、后两种不同的α-受体。例如,甲氧胺、新福林选择性地激动α_1-受体;可乐宁(clonidine)、托马唑啉(tramazoline)选择性地激动α_2-受体。哌唑嗪(prazosin)主要阻断α_1-受体;育亨宾(yohimbine)主要阻断α_2-受体。在大多数血管,NA激活突触后α-受体,使血管平滑肌收缩,并因此使血管收缩。但并非所有血管平滑肌细胞上的α-受体均属同一亚型。多数离体动脉平滑肌对A、甲氧胺、NA新福林等α-激动剂发生收缩反应,但对可乐宁和托马唑啉相
Numerous experiments have shown that the adrenergic neuro-effector contacts differ in their a-receptors on the presynaptic and postsynaptic membranes, and Langers first proposed that the post-synaptic a-receptor that regulates effector responses is named α_1 -receptors, whereas the [alpha] -receptors that regulate the release of NA on the presynaptic membrane are termed [alpha] 2-receptors. Some drugs selectively activate or block the presynaptic and post two different alpha-receptors. For example, methoxylamine, neoprene selectively activates the alpha 1-receptor; clonidine, tramazoline selectively activates the alpha 2 -receptors. Prazosin mainly blocks α 1 -receptors; yohimbine mainly blocks α 2 -receptors. In most blood vessels, NA activates the postsynaptic [alpha] -receptors, causing contraction of the vascular smooth muscle and therefore vasoconstriction. However, not all a-receptors on vascular smooth muscle cells are of the same subtype. Most isolated arterial smooth muscle contractile responses to α-agonists such as A, methoxyamine, NA neoformans, but the effects of clonidine and tomazoline phase