Atrial natriuretic peptide and patent ductus arteriosus

normal healthy children.4 The association between the fall in atrial natriuretic peptide concentration and decrease in body weight after volume reduction by haemodialysis suggests that in children volume expansion releases atrial natriuretic peptide. In preterm infants plasma atrial natriuretic peptide concentrations are considerably raised on the second day of life and decrease to normal within 2 or 3 weeks of age.S Concentrations are raised in premature infants with increased sodium intake and are related to sodium excretion.6 The localisation of the sensor of atrial natriuretic peptide release has not yet been clearly defined in clinical studies. Interruption of left to right shunting and decreased left atrial distension by surgical closure of the patent ductus arteriosus seems to be a good clinical model in which to study mechanisms of atrial natriuretic peptide release in preterm infants. The immediate drop in plasma atrial natriuretic peptide concentration by 72% when the ductus is closed in preterm infants may indicate that atrial distension due to left to right shunting is responsible for increased atrial natriuretic peptide release in preterm infants with patent ductus arteriosus. Raised plasma atrial natriuretic peptide concentrations in preterm infants with patent ductus arteriosus may help to preserve renal function and to antagonise the renal vasoconstrictor hormones that are raised in preterm infants with symptomatic patent ductus arteriosus. Although we did not measure renal function in the present study, indirect evidence (unchanged body weight and stable plasma concentrations of sodium, protein, and creatinine) suggest that an appreciable reduction in urine flow did not occur in our preterm infants after closure of the ductus. This may be due to the fact that renal vasoconstrictor hormone concentrations fall at the same time and renal perfusion improves after abolishing the ductal steal phenomenon.