Trachte G J
Department of Pharmacology, University of Minnesota-Duluth, School of Medicine.
J Pharmacol Exp Ther. 1988 Jul;246(1):211-7.
The effect of sympathectomy and norepinephrine depletion on prostaglandin (PG) synthesis in response to angiotensins II and III was examined in isolated vasa deferentia of the rabbit. Either 6-hydroxydopamine or surgical denervation significantly depressed norepinephrine concentrations in the vas deferens relative to contralateral controls, thus confirming an effective sympathectomy. Guanethidine also resulted in a significant reduction in norepinephrine concentrations in the vas deferens. Base-line PGE production by the vasa deferentia was not altered by guanethidine but was attenuated by 6-hydroxydopamine and increased by surgical denervation. All the treatments reduced angiotensin-induced PGE synthesis. The effect of denervation on PGE synthesis was greater than that of norepinephrine depletion. We interpret these results to indicate that angiotensins stimulate PGE production by adrenergic nerves in the vas deferens and that released norepinephrine mediates a part of the PGE production in response to the angiotensins. The 6-hydroxydopamine experiments are consistent with the adrenergic nerves being the predominant source of PGE in this preparation.
在兔离体输精管中，研究了交感神经切除术和去甲肾上腺素耗竭对血管紧张素II和III刺激下前列腺素（PG）合成的影响。相对于对侧对照，6-羟基多巴胺或手术去神经支配均显著降低了输精管中的去甲肾上腺素浓度，从而证实交感神经切除术有效。胍乙啶也导致输精管中去甲肾上腺素浓度显著降低。胍乙啶未改变输精管的基础PGE生成，但6-羟基多巴胺使其减弱，而手术去神经支配使其增加。所有处理均降低了血管紧张素诱导的PGE合成。去神经支配对PGE合成的影响大于去甲肾上腺素耗竭。我们将这些结果解释为表明血管紧张素刺激输精管中肾上腺素能神经产生PGE，并且释放的去甲肾上腺素介导了部分对血管紧张素的PGE生成反应。6-羟基多巴胺实验与肾上腺素能神经是该制剂中PGE的主要来源一致。
