Limberger N, Funk L, Trendelenburg A U, Starke K
Pharmakologisches Institut, Freiburg, Germany.
Naunyn Schmiedebergs Arch Pharmacol. 1995 Jul;352(1):31-42. doi: 10.1007/BF00169187.
The study was devised to classify, by means of antagonist affinities, the presynaptic alpha 2-autoreceptors of rabbit atria and kidney in terms of alpha 2A, alpha 2B, alpha 2C and alpha 2D. A set of antagonists was chosen that was able to discriminate between the four subtypes. Small pieces of the left atrium and slices of the kidney cortex were preincubated with 3H-noradrenaline and then superfused and stimulated electrically. In one series of experiments, tissue pieces were stimulated by relatively long pulse trains (1 or 2 min) leading to alpha 2-autoinhibition. All 11 (atria) or 10 (kidney) antagonists increased the evoked overflow of tritium. pEC30% values (concentrations causing 30% increase) were interpolated from concentration-response curves. In a second series of experiments, tissue pieces were stimulated by brief pulse trains (0.4 s) that did not lead to alpha 2-autoinhibition, and concentration-inhibition curves of the alpha 2-selective agonist 5-bromo-6-(2-imidazolin-2-ylamino)-quinoxaline (UK 14,304) were determined. Most of the 11 (atria) or 8 (kidney) antagonists shifted the concentration-inhibition curve of UK 14,304 to the right. pKd values of the antagonists were calculated from the shifts. pEC30% values correlated with pKd values, both in atria (r = 0.728) and in the kidney (r = 0.930). pEC30% values in atria correlated with pEC30% values in the kidney (r = 0.988) and pKd values in atria correlated with pKd values in kidney (r = 0.923). It is concluded that the alpha 2-autoreceptors in atria and the kidney are the same. Comparison with antagonist affinities for prototypic native alpha 2 binding sites, alpha 2 binding sites in cells transfected with alpha 2 subtype genes, and previously classified presynaptic alpha 2-adrenoceptors--all taken from the literature--indicates that both autoreceptors are alpha 2A. This conclusion is reached with either of the two independent estimates of autoreceptor affinity, pEC30% and pKd. The results are compatible with the hypothesis that at least the majority of alpha 2-autoreceptors belong to the alpha 2A/D branch of the alpha 2-adrenoceptor tree, across mammalian or at least rodent and lagomorph species.
该研究旨在通过拮抗剂亲和力,依据α2A、α2B、α2C和α2D对兔心房和肾脏的突触前α2 - 自身受体进行分类。选择了一组能够区分这四种亚型的拮抗剂。将小块左心房和肾皮质切片与3H - 去甲肾上腺素预孵育,然后进行灌流并电刺激。在一系列实验中,组织块通过相对较长的脉冲串(1或2分钟)进行刺激,从而导致α2 - 自身抑制。所有11种(心房)或10种(肾脏)拮抗剂均增加了诱发的氚溢出。pEC30%值(引起30%增加的浓度)从浓度 - 反应曲线中插值得到。在第二系列实验中,组织块通过短暂脉冲串(0.4秒)进行刺激,该脉冲串不会导致α2 - 自身抑制,并测定了α2 - 选择性激动剂5 - 溴 - 6 - (2 - 咪唑啉 - 2 - 基氨基) - 喹喔啉(UK 14,304)的浓度 - 抑制曲线。11种(心房)或8种(肾脏)拮抗剂中的大多数将UK 14,304的浓度 - 抑制曲线向右移动。拮抗剂的pKd值根据移动情况计算得出。pEC30%值与pKd值相关,在心房中(r = 0.728)以及在肾脏中(r = 0.930)均如此。心房中的pEC30%值与肾脏中的pEC30%值相关(r = 0.988),心房中的pKd值与肾脏中的pKd值相关(r = 0.923)。结论是心房和肾脏中的α2 - 自身受体是相同的。与来自文献的原型天然α2结合位点、用α2亚型基因转染的细胞中的α2结合位点以及先前分类的突触前α2 - 肾上腺素能受体的拮抗剂亲和力进行比较表明,两种自身受体均为α2A。该结论是通过对自身受体亲和力的两种独立估计值pEC30%和pKd中的任何一种得出的。结果与以下假设相符,即至少大多数α2 - 自身受体属于α2 - 肾上腺素能受体树的α2A/D分支,跨越哺乳动物或至少啮齿动物和兔形目物种。