调查神经传递的输精管α(2 a / D)肾上腺素能受体基因敲除小鼠。

文章的细节

引用

复制到剪贴板

Docherty佳L, Vandeputte C, JR .

调查神经传递的输精管α(2 a / D)肾上腺素能受体基因敲除小鼠。

Br J杂志。2002年7月,136 (6):857 - 64。

PubMed ID

12110610 (在PubMed

]

文摘

1。我们已经调查了预处理和post-junctional响应输精管从野生型和α(2 a / D)肾上腺素能受体基因敲除小鼠。一个刺激的反应没有显著不同野生型和小鼠。等长收缩到10赫兹的4 s明显更大的刺激从淘汰赛与野生型相比输精管。2。育亨宾的最大10 Hz stimulation-evoked收缩增强作用是206.2 + / - -38.0%的控制在野生型,但在淘汰赛135.8 + / - -13.6%的控制。阿尔法(2 a / D)肾上腺素能受体选择性拮抗剂BRL 44408显著增加了10 Hz stimulation-evoked收缩在野生型而不是击倒,相反的是真正的为α肾上腺素能受体选择性拮抗剂spiroxatrine (2 c)。α肾上腺素受体拮抗剂(2 b)对诱发imiloxan没有影响收缩除了在高浓度时,只有在野生型。可卡因后(3 microM)和BRL 44408 (1 microM) 10 Hz反应相似的形状和最大的野生型和淘汰赛之间。3所示。 The alpha(2)-adrenoceptor agonist xylazine virtually abolished the early component of the contraction to 10 Hz stimulation in the presence of nifedipine (10 microM) in vas deferens from knockout mice in a way consistent with a change of receptor subtype but without clear evidence for a reduced receptor number. However, the late component of the contraction to 10 Hz stimulation was significantly potentiated by xylazine in tissues from knock-out mice. 4. It is concluded that, although non-alpha(2A/D)-adrenoceptors replace alpha(2D)-adrenoceptors in this knockout, the alpha(2)-adrenoceptor agonist and antagonist data are contradictory. The antagonist data suggest a major loss of prejunctional alpha(2)-adrenoceptors, but this is not necessarily supported by the agonist data.

beplay体育安全吗DrugBank数据引用了这篇文章

药物靶点

药物	目标	类	生物	药理作用	行动
育亨宾	Alpha-2B肾上腺素能受体	蛋白质	人类	是的	拮抗剂	细节
育亨宾	Alpha-2C肾上腺素能受体	蛋白质	人类	是的	拮抗剂	细节