Hemodynamic and humoral effects of prostaglandin inhibition in exercising humans.
This double-blind placebo-controlled study investigated whether indomethacin-induced (500 mg/3 days) prostaglandin synthesis inhibition (PG inhibition) affected systemic hemodynamics and several humoral factors in nine sodium-replete normal humans, during exercise. Independent of the level of physical activity, PG inhibition was accompanied by small but significant (P less than 0.001) increases in systolic (+4.3 mmHg) and diastolic (+1.8 mmHg) intra-arterial pressure: the changes in cardiac output (determined noninvasively), systemic vascular resistance, and exercise capacity did not reach a level of statistical significance. After PG inhibition, plasma 13,14-dihydro-15-keto/prostaglandin F2 alpha, plasma renin, and aldosterone were reduced (P less than 0.001) at rest sitting and exercise, but PG inhibition did not prevent the exercise-induced stimulation of the plasma renin-aldosterone system. The urinary sodium excretion, averaging 156 meq/24 h during placebo, decreased (P less than 0.001) by 28 meq/24 h during PG inhibition: urinary aldosterone and kallikrein and the plasma catecholamines remained unchanged. In resting and exercising sodium-replete subjects, prostaglandins seem to exert a depressor effect on the systemic circulation and to increase plasma renin activity, but they are probably not involved in the exercise-related stimulation of the plasma renin-aldosterone system.
D000328:Adult; D000450:Aldosterone / Q000097:blood; D016861:Cyclooxygenase Inhibitors; D004837:Epinephrine / Q000097:blood; D006439:Hemodynamics; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D010101:Oxygen Consumption; D005082:Physical Exertion; D012083:Renin / Q000097:blood; D012119:Respiration; D012964:Sodium / Q000652:urine
D016861:Cyclooxygenase Inhibitors; D000450:Aldosterone; D012964:Sodium; D012083:Renin; D007213:Indomethacin; D004837:Epinephrine