Renal prostaglandin E2 and F2?? synthesis during exercise

Abstract

To assess the effects of acute exercise on renal prostaglandins E2 (PGE2) and F2 alpha (PGF2 alpha) synthesis, urine collections were obtained from six women before and after 30 min of treadmill exercise at approximately 80% of their maximal oxygen consumption. After receiving a placebo for 3 days, with acute exercise, there was a significant increase only in recovery urine PGE2 concentration. Due to a decline in urine volume, PGF2 excretion was unchanged and PGF2 alpha excretion was significantly decreased by exercise. Subjects repeated the tests after 3 d of indomethacin treatment (150 mg X d-1), a known renal prostaglandin (PG) inhibitor, and 3 d of sulindac (300 mg X d-1), a non-steroidal anti-inflammatory drug which may not inhibit renal PG synthesis. Pre-exercise urine PGE2 concentrations were decreased by indomethacin but not by sulindac, whereas, PGF2 alpha concentrations were decreased by both drugs. When compared to the control test, indomethacin and sulindac had different effects on pre-exercise urine/plasma osmolality ratios and free water clearances. Neither indomethacin nor sulindac influenced the decreases in free water clearances, which were observed during the placebo tests. Exercise proteinuria was significantly increased by indomethacin but not by sulindac. In conclusion, these data demonstrate that acute exercise may stimulate renal PGE2 synthesis. During exercise, renal PG synthesis attenuates protein excretion. There also appear to be differences between indomethacin and sulindac with regard to the effects on renal PG synthesis and kidney function.