Furosemide-induced alterations in the electrolyte status, the function of renin-angiotensin-aldosterone system, and the urinary excretion of prostaglandins in newborn infants.

To assess the responsiveness of the renin-angiotensin-aldosterone system of the neonate to acute furosemide stimulation and the role of renal prostaglandins 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 aldosterone, prostaglandin E, and prostaglandin F2 alpha excretion 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 less than 0.001), urinary sodium (P less than 0.001), potassium (P less than 0.05), and chloride (P less than 0.001) excretion increased significantly. Furosemide administration also resulted in a significant increase from 4.41 +/- 2.00 to 9.70 +/- 2.32 ng/ml/hr (P less than 0.02) in plasma renin activity, from 1.17 +/- 0.22 to 1.68 +/- 0.36 ng/ml (P less than 0.025) in plasma aldosterone, from 0.93 +/- 0.16 to 1.53 +/- 0.35 microgram/12 hr (P less than 0.025) in urinary aldosterone, from 17.53 +/- 3.37 to 23.73 +/- 3.16 ng/12 hr (P less than 0.025) in prostaglandin E, and from 16.48 +/- 4.12 to 26.27 +/- 4.12 ng/12 hr (P less than 0.05) in prostaglandin F2 alpha. 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.