Abstract
In 12 human volunteers, indomethacin inhibited renal prostaglandin [PG] production as reflected by RIA [radioimmunoassay] of urinary PGE2. The increases in plasma renin activity and plasma and urinary aldosterone following acute furosemide challenge were markedly blunted in the presence of indomethacin. In light of recent developments indicating an intimate relationship between PG and renin release, these results provide further evidence for a pivotal role of renal PG in modulating the responsiveness of the renin-angiotensin-aldosterone axis in man.

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