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Contribution of prostaglandins to the systemic and renal vascular response to frusemide in normal man.
Author(s) -
Mackay IG,
Muir AL,
Watson ML
Publication year - 1984
Publication title -
british journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.216
H-Index - 146
eISSN - 1365-2125
pISSN - 0306-5251
DOI - 10.1111/j.1365-2125.1984.tb02383.x
Subject(s) - furosemide , plasma renin activity , endocrinology , renal blood flow , metabolite , medicine , renal function , excretion , chemistry , urine , natriuresis , prostaglandin , urinary system , effective renal plasma flow , diuresis , pharmacology , renin–angiotensin system , blood pressure
In eight normotensive male volunteers indomethacin decreased both the peak urine flow rate and total sodium excreted within 1 h of an intravenous dose of frusemide. Resting effective renal plasma flow and glomerular filtration rate were unchanged by indomethacin, but the increase in both parameters after frusemide was inhibited. The early increase in plasma renin activity after frusemide was inhibited by indomethacin. Indomethacin decreased urinary excretion of PGE by 80% and the increase after frusemide was abolished. The urinary excretion of a metabolite of systemic PGI2 was unaltered in the 40‐60 min period following frusemide. The early haemodynamic effects of frusemide are likely to be prostaglandin mediated, but there was no evidence of any change in systemic PGI2 synthesis after frusemide.