Hedqvist P
Prostaglandins. 1979 Feb;17(2):249-58. doi: 10.1016/0090-6980(79)90045-5.
In the Tyrode's perfused rabbit kidney PGI2 (1.3 x 10(-8)-3.3 x 10(-7)M) dose-dependently inhibited vasoconstrictor responses to sympathetic nerve stimulation, as did PGE2. The dose-effect curve of the two compounds differed, making PGI2 the less potent in the low concentration and the more potent in the high. PGI2 also inhibited the vasoconstrictor response to exogenous noradrenaline, but it had no effect on transmitter release. The main metabolite of PGI2, 6-keto-PGF1 alpha, was ineffective both on noradrenaline release and on vascular responses to nerve stimulation or exogenous noradrenaline. It is suggested that PGI2, if a significant renal prostaglandin, may modulate renal neuroeffector transmission post-junctionally, thereby forming a complement to the prejunctional action of PGE2.
在台氏液灌注的兔肾中，前列环素（PGI2，浓度为1.3×10⁻⁸ - 3.3×10⁻⁷M）与前列腺素E2（PGE2）一样，对交感神经刺激引起的血管收缩反应具有剂量依赖性抑制作用。这两种化合物的剂量 - 效应曲线不同，使得PGI2在低浓度时效力较低，而在高浓度时效力较高。PGI2还抑制对外源性去甲肾上腺素的血管收缩反应，但对递质释放没有影响。PGI2的主要代谢产物6 - 酮 - 前列腺素F1α对外源性去甲肾上腺素的释放以及对神经刺激或外源性去甲肾上腺素引起的血管反应均无作用。提示如果PGI2是肾内一种重要前列腺素，它可能在神经效应器接头后调节肾神经传递，从而对PGE2的接头前作用起到补充作用。
