[Effect of arginine-vasopressin infusion on the secretion of tracheal fluid in sheep fetuses].

Timely evacuation of alveolar fluid, release of surfactant and the beginning of continuous breathing, are key processes for an adequate adaptation of the fetus to the extrauterine life. Fetal vasopressin increases during labor and inhibit the secretion of tracheal fluid through a mechanism still unknown. The aim of this study was to elucidate the mechanism whereby vasopressin inhibit the secretion of lung fluid. We used fetal sheep chronically catheterized and infused either with vasopressin, vasopressin agonist (V2; dDAVP) or vasopressin antagonist (V1). Tracheal flow was measured during basal and infusions periods of 2 hours, monitoring fetal blood pressure, heart rate and blood pH and gases. Vasopressin and the V1 vasopressin antagonist caused a significant reduction in tracheal fluid flow, effect that was potentiated when both peptides were infused together. The V2 vasopressin agonist had no effect on the secretion of lung fluid. We concluded that vasopressin causes a significant inhibition of lung liquid secretion through a mechanism different to the activation of V1 and V2 receptors, and we propose the existence of other (s) kind of receptors (or receptors) for vasopressin that is (are) active during fetal life.