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Effects of Low‐Dose Aspirin on Responses to Furosemide
Author(s) -
Wilson Thomas W.,
McCauley Frances A.,
Wells Holly D.
Publication year - 1986
Publication title -
the journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.92
H-Index - 116
eISSN - 1552-4604
pISSN - 0091-2700
DOI - 10.1002/j.1552-4604.1986.tb02915.x
Subject(s) - furosemide , aspirin , plasma renin activity , endocrinology , medicine , diuretic , excretion , thromboxane , thromboxane b2 , chemistry , pharmacology , renin–angiotensin system , platelet , blood pressure
We assessed the effects of low‐dose aspirin (0.5 and 15 mg/kg/d) on renal prostaglandin synthesis and action in healthy volunteers using intravenous furosemide as a stimulus. Inhibition of platelet cyclo‐oxygenase was assessed by changes in serum thromboxane B 2 (TXB 2 ) level. After one week of treatment, ten healthy subjects did not show any change in weight, blood pressure, or diuretic and natriuretic responses to furosemide with either dose of aspirin. Serum TXB 2 level was reduced to 3% of control by aspirin 0.5 mg/kg/d and to 0.1% by the higher dose. In contrast, urine excretion of TXB 2 was only reduced to 68% and 51% of the placebo value, whereas 6‐keto‐prostaglandin F 1α (6kPGF 1α ) excretion was not decreased by either dose. Furosemide produced a transient increase in excretion rates of TXB 2 and 6kPGF 1α that was of lesser duration than the diuretic response. These transient increases were slightly reduced by aspirin. Baseline plasma renin activity was not affected by either dose of aspirin. The brisk increment in plasma renin activity seen ten minutes after furosemide, as well as later values (30 and 240 min) were not changed by aspirin. We conclude that chronic low‐dose aspirin can profoundly affect platelet PG production without affecting stimulated renal PGI 2 production or plasma renin activity. There is a modest reduction in urine TXB 2 excretion that is consistent with a primarily renal source of this metabolite.