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A major function of the pulmonary alveolar type II cell is the secretion of surfactant, a lipoprotein-like substance, via exocytosis of secretory vesicles termed lamellar bodies (LBs). The process of surfactant secretion is remarkable in several aspects, considering stimulus-delayed fusion activity, poor solubility of vesicle contents, long hemifusion lifetimes, slow fusion pore expansion and active, actin-driven content release. Cell stretch as well as P2Y(2) receptor stimulation by extracellular ATP are considered the most potent stimuli for LB exocytosis. For both stimuli, elevation of the cytoplasmic Ca(2+) concentration [Ca(2+)](c) is a key step. This review summarizes possible physiological roles and pathways of stretch- or ATP-induced surfactant secretion and discusses molecular mechanisms controlling the pre-, hemi- and postfusion phase, in comparison with neuroendocrine release mechanisms.

Lamellar Body Exocytosis by Cell Stretch or Purinergic Stimulation: Possible Physiological Roles, Messengers and Mechanisms