Hypertension, Vol 8, 677-684, Copyright © 1986 by American Heart Association
LM Ruilope, R Garcia Robles, C Paya, JM Alcazar, E Miravalles, J Sancho-Rof, J Rodicio, FG Knox and JC Romero
The prolonged effects (42 days) of indomethacin treatment on the renin-
angiotensin-aldosterone axis, renal hemodynamics, and renal excretory
function in humans were studied. Indomethacin produced a 41% sustained
depression in the 24-hour excretion of prostaglandin E2 and a mild (7%)
decrease in inulin clearance but did not affect the clearance of p-
aminohippurate, the 24-hour excretion of sodium and potassium, or the basal
values of plasma aldosterone; however, it decreased the basal values of
renin and prevented the stimulated (3 hours of walking) responses of plasma
renin activity and plasma aldosterone. Indomethacin also produced a
decrease in both the diuretic and saluretic response to furosemide and in
the renal ability to concentrate urine. The indomethacin-induced
hyporeninism and hypoaldosteronism were more pronounced when the subjects
were receiving a sodium-restricted diet. This finding indicates that
prolonged administration of anti- inflammatory drugs induces chronic
hyporeninism and hypoaldosteronism. Prolonged treatment with indomethacin
also produced some of the symptoms of a syndrome of hypoprostaglandinism,
such as decreased plasma renin activity, plasma aldosterone, and urinary
prostaglandin E2 in association with increases in plasma potassium levels
and diastolic pressure.
ARTICLES
Effects of long-term treatment with indomethacin on renal function
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