Furosemide-induced Alterations in the Electrolyte Status, the Function of Renin-Angiotensin-Aldosterone System, and the Urinary Excretion of Prostaglandins in Newborn Infants

Summary: To assess the responsiveness of the renin-angiotensin-aldoste-rone system of the neonate to acute furosemide stimulation and the role of renal prostagladias in mediating the response of the renin-angiotensin-aldosterone system, this study was carried out to determine simultaneously plasma renin activity, plasma aldosterone concentration, urinary abosteroae. prostaglandin E, and prostaglandin F2aexcretion along with determination of plasma electrolyte concentration and urinary electrolyte excretion.Measurements were made on 19 newborn infants with mean birth weight and gestational age of 3009 g (range, 2700 to 4150 g) and 38.7 wk (range, 36 to 41 wk) at the age of 4 to 7 days before and after IM administration of furosemide in a dose of 1 mg/kg.It was demonstrated that in response to furosemide, urine volume (P < 0.001). urinary sodium (P < 0.001). potassium (P < OM), and chloride (P < 0.001) excretion increased significantly.Furosemide administration also resulted in a significant increase from 4.41 f 2.00 to 9.70 f 2.32 ng/ml/hr (P < 0.02) in plasma renin activity, from 1.17 f 0.22 to 1.68 2 0.36 ng/ml (P < 0.025) in plasma aldosterone, from 0.93 f 0.16 to 1.53 f 0.35 pg/12 hr (P < 0.025) in urinary aldosterone, from 17.53 f 3.37 to 23.73 f 3.16 4 1 2 hr (P < 0.025) in prostaglandin E, and from 16.48 2 4.12 to 26.27 2 4.12 ng/l2 hr (P < 0.05) in prostaglandin Fz,.It is concluded that the renin-angiotensin-aldosterone system of the neonate responds to acute furosemide challenge in spite of its high baseline activity, and its response may be mediated by increased renal prostaglandin production.Speculation: The demonstration of high basal activity of the renin-angiotensin-aldosterone system in "nonstimulated" healthy newborn infants prompted us to study whether this high baseline activity is or is not a rate-limiting determinant of the responsiveness of the renin-angiotensin-aldosterone system to furosemide stimulation. It is also to be clarified whether the increase in the activity of the renin-angiotensin-aldosterone system, if any, in response to furosemide administration could be ascribed to its direct effect on renal sodium transport and renal hemodynamics or whether it might be mediated by the furosemide-induced alterations in renal prostaglandin production.