Endogenously synthesized prostaglandins stimulate sympathetic nervous system activity.
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.
D000818:Animals; D007213:Indomethacin / Q000494:pharmacology; D008676:Metanephrine / Q000652:urine; D008734:Methoxyhydroxyphenylglycol / Q000652:urine; D009647:Normetanephrine / Q000652:urine*; D011191:Potassium Deficiency / Q000378:metabolism; D011453:Prostaglandins / Q000096:biosynthesis*; D051381:Rats; D011916:Rats, Inbred F344; D012083:Renin / Q000097:blood; D013564:Sympathetic Nervous System / Q000502:physiology*
D011453:Prostaglandins; D009647:Normetanephrine; D008676:Metanephrine; D008734:Methoxyhydroxyphenylglycol; D012083:Renin; D007213:Indomethacin