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Renal function and tubular transport effects of sulindac and naproxen in chronic heart failure
Author(s) -
Eriksson LarsOlof,
Beermann B,
Kallner Mora
Publication year - 1987
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1038/clpt.1987.213
Subject(s) - sulindac , furosemide , renal function , naproxen , renal blood flow , aldosterone , medicine , plasma renin activity , effective renal plasma flow , endocrinology , free water clearance , prostacyclin , renal circulation , chemistry , heart failure , urology , renin–angiotensin system , blood pressure , alternative medicine , pathology , nonsteroidal
Renal function and excretion of water, salt, and the prostacyclin hydration product (6‐keto‐PGF 1α ) were evaluated in 10 furosemide‐treated patients with well‐controlled congestive heart failure. Four doses of sulindac (200 mg b.i.d.) and naproxen (500 mg b.i.d.) were given every 12 hours in a double‐blind crossover design. Naproxen significantly decreased the urinary excretion of water (19%), sodium (26%), chloride (26%), and 6‐keto PGF 1α (76%) and decreased osmolal clearance (18%). No significant changes in these functions were observed in the patients receiving sulindac. Plasma renin activity, plasma aldosterone, freewater clearance, or clearance of furosemide did not change significantly with either treatment. Although the basal glomerular filtration rate (GFR) and renal plasma flow (RPF) were reduced, these patients with cardiac disease, with normal serum sodium concentration, did not have any further reduction of GFR or RPF despite naproxen‐induced inhibition of renal prostacyclin synthesis. It is concluded that renal prostaglandins contribute to the natriuretic effect of oral furosemide in patients with compensated congestive heart failure. In this clinical setting, GFR and RPF are not critically dependent on intact renal PGI 2 synthesis. The lack of effect on renal prostaglandin synthesis and the renal response to oral furosemide supports the concept of a renal sparing effect of sulindac. Clinical Pharmacology and Therapeutics (1987) 42 , 646–654; doi: 10.1038/clpt.1987.213