Yasuda G, Misu Y
Department of Pharmacology, Yokohama City University School of Medicine, Japan.
Jpn J Pharmacol. 1988 Sep;48(1):153-6. doi: 10.1254/jjp.48.153.
Effects of some prostaglandins (PGs) on adrenergic transmission were studied in guinea pig pulmonary arteries preloaded with 3H-norepinephrine. PGE1 and PGE2 at 0.1 to 100 nM concentration-dependently inhibited 3H-release and contraction evoked at 5 Hz. This inhibition was antagonized by diphloretin phosphate. PGF2 alpha at 1 to 100 nM had no effect on evoked 3H-release and contraction. PGI2 at 1 to 100 nM also failed to modify evoked 3H-release, but markedly and concentration-dependently decreased evoked contraction. There exist presynaptic inhibitory PGE1 and PGE2 receptive sites on adrenergic neurons innervating guinea pig pulmonary arteries, whereas PGF2 alpha and PGI2 produced no effect on the adrenergic neurons.
在预先用3H-去甲肾上腺素加载的豚鼠肺动脉中研究了一些前列腺素(PGs)对肾上腺素能传递的影响。浓度为0.1至100 nM的PGE1和PGE2以浓度依赖性方式抑制5 Hz诱发的3H释放和收缩。这种抑制作用被磷酸二氢黄酮拮抗。浓度为1至100 nM的PGF2α对诱发的3H释放和收缩没有影响。浓度为1至100 nM的PGI2也未能改变诱发的3H释放,但显著且浓度依赖性地降低了诱发的收缩。在支配豚鼠肺动脉的肾上腺素能神经元上存在突触前抑制性PGE1和PGE2受体位点,而PGF2α和PGI2对肾上腺素能神经元没有影响。