Factors regulating the release of phosphatidylcholine (PC) from neonatal-rat lungs were investigated. The results show that the release of prelabelled PC from the newborn-rat lung was augmented by air ventilation at the onset of breathing. This response was mimicked in lungs of pups delivered 1 day before term and allowed to breathe for different time intervals. Anoxia further augmented the ventilation-enhanced PC release from the newborn-rat lungs. The ventilation-induced release of PC was not abolished by the prior treatment of pups in utero or mothers in vivo with phenoxybenzamine, propranolol or atropine, suggesting the lack of receptor stimulation in the ventilation-enhanced PC release at birth. The results also show that ventilation stimulated [methyl-14C]choline incorporation into lung PC, presumably to replenish the depleted surfactant stores. The ratio of adenylate cyclase/cyclic AMP phosphodiesterase activities, which reflects cyclic AMP levels in the developing rat lungs, did not change during the 120 min of air ventilation when the release of PC was much enhanced, implying that cyclic AMP may not be involved. This confirms our conclusion that stimulation of beta-adrenergic receptor was not involved in the air-ventilation-enhanced release of PC. Since the cell number or size did not change during 120 min of ventilation when the alveolar-cell surface was maximally distended, it is suggested that distension of alveolar wall by air ventilation at the onset of breathing may bring the lamellar bodies containing surfactant close to the luminal surface of alveolar type II cells, thereby enhancing their fusion and extrusion by exocytosis.

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