Verbeuren T J, Jordaens F H, Zonnekeyn L L, Herman A G
Arch Int Pharmacodyn Ther. 1986 Nov;284(1):38-52.
In segments of isolated dog saphenous veins, S-3341 (10(-8) to 10(-4) M) induced concentration-dependent contractions which, like those to clonidine, were progressively inhibited by increasing concentrations of yohimbine (10(-8) to 10(-6) M) but not by prazosin (10(-8) to 10(-6) M). In strips of the rabbit main pulmonary artery, previously labelled with [3H]noradrenaline and mounted for superfusion, S-3341 and clonidine both decreased the overflow of [3H] caused by electrical stimulation; these effects of S-3341 and clonidine were inhibited by 10(-6) M of yohimbine but not by 10(-6) M of prazosin. Our results illustrate that both S-3341 and clonidine cause contraction by activation of postjunctional alpha 2-adrenoceptors and decrease noradrenaline-release by stimulating prejunctional alpha 2-adrenoceptors. At the postjunctional alpha 2-adrenoceptors clonidine is 27 times more potent than S-3341, while at the prejunctional alpha 2-adrenoceptors, clonidine is only 15 times more potent than S-3341.
在分离的犬隐静脉段中，S - 3341（10⁻⁸至10⁻⁴M）引起浓度依赖性收缩，与可乐定引起的收缩一样，随着育亨宾浓度增加（10⁻⁸至10⁻⁶M），这种收缩逐渐受到抑制，但哌唑嗪（10⁻⁸至10⁻⁶M）则无此作用。在预先用[³H]去甲肾上腺素标记并安装用于灌注的兔主肺动脉条中，S - 3341和可乐定均降低电刺激引起的[³H]溢出；S - 3341和可乐定的这些作用被10⁻⁶M育亨宾抑制，但不被10⁻⁶M哌唑嗪抑制。我们的结果表明，S - 3341和可乐定均通过激活节后α₂ - 肾上腺素能受体引起收缩，并通过刺激节前α₂ - 肾上腺素能受体减少去甲肾上腺素释放。在节后α₂ - 肾上腺素能受体上，可乐定的效力比S - 3341强27倍，而在节前α₂ - 肾上腺素能受体上，可乐定的效力仅比S - 3341强15倍。
