Robie N W
Am J Physiol. 1980 Sep;239(3):H422-6. doi: 10.1152/ajpheart.1980.239.3.H422.
The functional significance of presynaptic alpha-receptor modulation of sympathetic nerves was examined in vivo in the canine renal vascular bed. In pentobarbital-anesthetized dogs, the vasoconstrictor response to renal nerve stimulation and exogenous norepinephrine was compared before and during intra-arterial infusions of epinephrine, oxymetazoline, clonidine, and norepinephrine. Only epinephrine produced a modest decrease in stimulation-induced vasoconstriction at 1 Hz. After pretreatment with desipramine, intra-arterial infusions of epinephrine or norepinephrine did not alter stimulation-induced vasoconstrictor responses relative to exogenous norepinephrine. Further, neither yohimbine nor phentolamine (10(-9) to 10(-3) g, intra-arterial) produced a distinctly increased vasoconstrictor response to nerve stimulation relative to exogenous norepinephrine. Thus, studies using alpha-receptor agonists, antagonists, and inhibition of neuronal uptake failed to reveal a physiologically significant alpha-receptor-mediated negative feedback mechanism for stimulation-induced vasoconstriction in the canine renal vascular bed.
在犬肾血管床中对交感神经突触前α受体调节的功能意义进行了体内研究。在戊巴比妥麻醉的犬中,比较了在动脉内输注肾上腺素、羟甲唑啉、可乐定和去甲肾上腺素之前和期间,肾神经刺激和外源性去甲肾上腺素引起的血管收缩反应。只有肾上腺素在1Hz时使刺激诱导的血管收缩有适度降低。在用地昔帕明预处理后,相对于外源性去甲肾上腺素,动脉内输注肾上腺素或去甲肾上腺素并未改变刺激诱导的血管收缩反应。此外,相对于外源性去甲肾上腺素,育亨宾或酚妥拉明(动脉内注射,10(-9)至10(-3)g)均未使神经刺激引起的血管收缩反应明显增加。因此,使用α受体激动剂、拮抗剂以及抑制神经元摄取的研究未能揭示犬肾血管床中刺激诱导的血管收缩存在生理上显著的α受体介导的负反馈机制。