Trendelenburg A U, Limberger N, Starke K
Pharmakologisches Institut, Freiburg, Germany.
Naunyn Schmiedebergs Arch Pharmacol. 1995 Jul;352(1):49-57. doi: 10.1007/BF00169189.
The study was devised to classify, by means of antagonist and agonist affinities, the presynaptic alpha 2-autoreceptors in guinea-pig heart atria and brain cortex in terms of alpha 2A, alpha 2B, alpha 2C and alpha 2D. A set of antagonists and agonists was chosen that was able to discriminate between the four subtypes. Small pieces of the atria and slices of the brain cortex were preincubated with 3H-noradrenaline and then superfused and stimulated electrically. In one series of experiments (atria only), tissue pieces were stimulated by relatively long pulse trains (1 min) leading to marked alpha 2-autoinhibition. All 10 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 (atria and brain slices), tissue pieces were stimulated by brief pulse trains (0.4 s or 40 ms) that led to little (atria) or no (brain slices) alpha 2-autoinhibition, and antagonist effects against the alpha 2-selective agonist 5-bromo-6-(2-imidazolin-2- ylamino)-quinoxaline (UK 14,304) were examined. All 10 (atria) or 8 (brain) antagonists shifted the concentration-inhibition curve of UK 14,304 to the right. pKd values of the antagonists were calculated from the shifts. In a third series of experiments (brain slices only), also with brief pulse trains (40 ms), pKa values (negative logarithms of dissociation constants of agonist-alpha 2-adrenoceptor complexes) were determined by comparison of concentration-inhibition curves of UK 14,304, guanoxabenz and oxymetazoline in normal tissue and in tissue in which a fraction of the receptors had been blocked by phenoxybenzamine.(ABSTRACT TRUNCATED AT 250 WORDS)
该研究旨在通过拮抗剂和激动剂亲和力,根据α2A、α2B、α2C和α2D对豚鼠心房和大脑皮层中的突触前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和激动剂。将心房小块和大脑皮层切片用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(仅心房)中,组织小块用相对较长的脉冲串(1分钟)刺激,导致明显的α2 - 自身抑制。所有10种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(心房和脑切片)中,组织小块用短暂的脉冲串(0.4秒或40毫秒)刺激,这导致很少(心房)或没有(脑切片)α2 - 自身抑制,并检测了拮抗剂对α2 - 选择性激动剂5 - 溴 - 6 -(2 - 咪唑啉 - 2 - 基氨基) - 喹喔啉(UK 14,304)的作用。所有10种(心房)或8种(脑)拮抗剂均将UK 14,304的浓度 - 抑制曲线右移。拮抗剂的pKd值根据位移计算得出。在第三系列实验(仅脑切片)中,同样使用短暂的脉冲串(40毫秒),通过比较UK 14,304、胍那苄和羟甲唑啉在正常组织和部分受体已被酚苄明阻断组织中的浓度 - 抑制曲线,测定pKa值(激动剂 - α2 - 肾上腺素能受体复合物解离常数的负对数)。(摘要截断于250字)