Güllner H G
Prostaglandins Leukot Med. 1983 Mar;10(3):345-8. doi: 10.1016/0262-1746(82)90089-0.
We examined the effect of an increase of endogenous prostaglandin production, induced by potassium depletion, on the urinary excretion of the norepinephrine metabolites metanephrine, normetanephrine and MHPG. Potassium deficiency caused a significant increase in all three metabolites. Treatment with indomethacin, 10 mg/day for 5 days, partially reversed the increase in the urinary excretion of norepinephrine metabolites. These findings suggest that in the intact organism prostaglandins stimulate, rather than inhibit norepinephrine release. Stimulation of prostaglandin synthesis may lead to an increase in sympathetic nervous system activity by a direct action or via a baroreceptor feedback mechanism.
我们研究了钾缺乏诱导的内源性前列腺素生成增加对去甲肾上腺素代谢产物间甲肾上腺素、去甲间甲肾上腺素和3-甲氧基-4-羟基苯乙二醇尿排泄的影响。钾缺乏导致所有这三种代谢产物显著增加。用吲哚美辛治疗，每天10毫克，持续5天，部分逆转了去甲肾上腺素代谢产物尿排泄的增加。这些发现表明，在完整机体中，前列腺素刺激而非抑制去甲肾上腺素释放。前列腺素合成的刺激可能通过直接作用或通过压力感受器反馈机制导致交感神经系统活动增加。
