Effect of sodium chloride supplementation on urinary endothelin-1 excretion in premature infants.

We investigated the role of endothelin-1 in the renal adaptation to alterations in sodium balance in premature infants. The postnatal course of urinary endothelin-1 excretion, an estimate of renal endothelin-1 production, was compared in premature infants receiving low or high sodium intake. Sodium supplementation was given in a dose of 3 to 5 mmol/kg per day and 1.5 to 2.5 mmol/kg per day at the postnatal ages of 8 to 21 and 22 to 35 days, respectively. Sodium balance and urinary endothelin-1 excretion were determined weekly up to the fifth week of life. Urinary endothelin-1 concentration (expressed in picomoles per liter) and urinary endothelin-1 excretion (expressed either in terms of picomoles per square meter per day or picomoles per millimole creatinine) were significantly lower in infants receiving a high sodium intake compared with those receiving low sodium intake (p < 0.001) in weeks 2 through 5. We conclude that in sodium-depleted premature infants with high urinary sodium excretion, an angiotensin II-mediated increase in renal endothelin-1 production occurs, which acts in concert with angiotensin II to restore sodium balance.

Role of atrial natriuretic peptide in sodium homeostasis in premature infants.

To examine the possible involvement of atrial natriuretic peptide (ANP) in sodium homeostasis in premature infants, two groups of low birth weight infants with different dietary sodium regimens were studied. Sodium balance and plasma concentration of ANP were measured at weekly intervals for 5 weeks. At 1 week of age the study was started by dividing infants into two groups, group 1 with low and group 2 with increased sodium intake. Mean plasma concentrations of ANP were 47.7 +/- 7.6 and 51.4 +/- 9.5 fmol/ml, respectively. A steady decrease in plasma ANP concentration to 18.8 +/- 2.9 fmol/ml was observed in infants with sodium intake 1.5 mmol/kg/d (group 1), which was related to the decrease in serum sodium concentration in this group. In contrast, supplementation with NaCl 4.6 mmol/kg/d (group 2) was associated with a 30% increase in plasma ANP concentration, significantly different (P less than 0.025) from that in infants not given supplement, and was also higher than the values in full-term neonates. Our data suggest that altered sodium homeostasis induces regulatory changes in plasma ANP levels. ANP may provide a sensitive and important hormonal system for the control of sodium balance, even in premature neonates.

Late hyponatremia in premature infants: role of aldosterone and arginine vasopressin.

To assess the possible involvement of arginine vasopressin in the pathogenesis of late hyponatremia in preterm infants, serial measurements of sodium balance, fractional sodium excretion, plasma and urine osmolality and sodium concentration, and urinary aldosterone and arginine vasopressin excretion were performed at weekly intervals in nine healthy preterm infants. During the course of late hyponatremia, there was a significant increase in urinary aldosterone and arginine vasopressin excretion, from 0.94 +/- 0.16 to 4.30 +/- 0.76 micrograms/day and from 0.38 +/- 0.08 to 1.19 +/- 0.26 ng/day, respectively, from the first to the fourth to fifth weeks. A significant negative correlation was found between fractional sodium excretion and urinary aldosterone excretion. Aldosterone excretion, however, correlated positively with urinary arginine vasopressin excretion in seven of the nine infants. The parallel increase in urinary aldosterone and arginine vasopressin excretion in salt-losing premature infants may occur in response to the protracted contraction of the extracellular fluid compartment, and may contribute to the restoration of volume in the body fluid compartments and to the development of late hyponatremia.

Postnatal development of renal sodium handling in premature infants.

To estimate the contribution of the specific defect in proximal and distal tubular reabsorption of sodium to renal salt wasting, fractional sodium excretion, distal tubular sodium delivery, and distal tubular sodium reabsorption were determined in 11 healthy premature infants. The study was performed on the seventh day and at weekly intervals thereafter up to the sixth week of life. Sodium clearance and fractional sodium excretion decreased significantly with increasing postnatal age (P less than 0.001). There was no significant alteration in either osmolar or free-water clearances. Distal tubular sodium delivery steadily decreased from 4.96 +/- 0.66 (mean +/- SE) in the first week to 3.3 +/- 0.41 ml/minute/dl GFR in the sixth week of life (P less than 0.05). Distal tubular sodium reabsorption was 69.5 +/- 2.36% in the first week, then rose significantly to reach a value of 83.7 +/- 1.85% in the second week (P less than 0.001) and remained practically unchanged thereafter. It is suggested that the rapid improvement of distal tubular sodium reabsorption in premature infants might result from forced stimulation by the excessively activated renin-angiotensin-aldosterone system.