Hesse I F, Johns E J
J Auton Pharmacol. 1984 Sep;4(3):145-52. doi: 10.1111/j.1474-8673.1984.tb00091.x.
An attempt has been made to classify the subtypes of alpha-adrenoreceptors mediating renal vasoconstriction in vivo using renal nerve stimulation and alpha-adrenoreceptor agonists and antagonists of varying selectivity in anesthetised rabbits. In the first series of experiments prazosin more potently inhibited the phenylephrine than the nerve induced renal vasoconstriction while phentolamine inhibited the response to phenylephrine and nerve stimulation nearly equally. In the second series of experiments low to moderate doses of yohimbine potently inhibited the renal vasoconstriction of clonidine, was less potent on that induced by noradrenaline and did not significantly affect that of phenylephrine. Prazosin was a potent antagonist of phenylephrine induced vasoconstriction but was less potent on nerve stimulation and noradrenaline, and was without effect on clonidine. In the third series of experiments, prazosin partially inhibited the renal vasoconstriction produced by all frequencies of nerve stimulation and that produced by high doses of noradrenaline. The prazosin resistant component of nerve stimulation and exogenous noradrenaline was significantly reduced by the addition of yohimbine. These results have been taken to suggest the presence of both alpha 1- and alpha 2-adrenoreceptors in the renal vasculature of the rabbit which mediate the renal vasoconstriction of exogenous and endogenous noradrenaline. They further show that in the rabbit the alpha 2-adrenoreceptors mediate a much greater proportion of the total renal vasoconstriction compared with the dog, cat or rat in which the alpha 1-adrenoreceptor population appears to be the predominant receptor.
研究人员尝试在麻醉兔身上，通过肾神经刺激以及使用不同选择性的α - 肾上腺素能受体激动剂和拮抗剂，对介导体内肾血管收缩的α - 肾上腺素能受体亚型进行分类。在第一组实验中，哌唑嗪对去氧肾上腺素诱导的肾血管收缩的抑制作用比对神经诱导的肾血管收缩更强，而酚妥拉明对去氧肾上腺素和神经刺激引起的反应的抑制作用几乎相同。在第二组实验中，低至中等剂量的育亨宾能有效抑制可乐定引起的肾血管收缩，对去甲肾上腺素诱导的肾血管收缩的抑制作用较弱，对去氧肾上腺素引起的肾血管收缩无显著影响。哌唑嗪是去氧肾上腺素诱导的血管收缩的有效拮抗剂，但对神经刺激和去甲肾上腺素的作用较弱，对可乐定无作用。在第三组实验中，哌唑嗪部分抑制了所有频率神经刺激引起的肾血管收缩以及高剂量去甲肾上腺素引起的肾血管收缩。加入育亨宾后，神经刺激和外源性去甲肾上腺素的哌唑嗪抗性成分显著降低。这些结果表明，兔肾血管系统中存在α1 - 和α2 - 肾上腺素能受体，它们介导外源性和内源性去甲肾上腺素引起的肾血管收缩。研究还进一步表明，与狗、猫或大鼠相比，兔体内α2 - 肾上腺素能受体介导的肾血管收缩在总肾血管收缩中所占比例更大，而在狗、猫或大鼠中，α1 - 肾上腺素能受体似乎是主要受体。
