Effects of Extracellular ATP on Surfactant Secretiona

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Abstract
Extracellular ATP is the most potent endogenous stimulus for surfactant phospholipid secretion from alveolar type II cells identified to date. This effect of ATP appears mediated via a P2-purinoceptor because the rank order of agonist potency is ATP greater than ADP greater than AMP = adenosine. Examination of other ATP analogues demonstrates a rank order of agonist potency of ATP = gamma S-ATP greater than AMPPNP greater than AMPPCP greater than AMPCPP for surfactant secretion, consistent with a P2y-purinoceptor mediating this effect. This hypothesis is further supported by experiments with reactive blue 2, which selectively inhibits ATP-stimulated surfactant phospholipid secretion and has been purported as a specific inhibitor at P2y-purinoceptors. Several second messenger systems are activated in the type II cell following agonist binding: intracellular Ca2+ is mobilized, prostaglandin levels increase, and protein kinase C is activated. Of these three second messengers, protein kinase C appears to be the most important for surfactant secretion because inhibition of protein kinase C activation blocks ATP-induced surfactant secretion whereas inhibition of Ca2+ mobilization and prostaglandin production does not affect ATP-induced surfactant secretion.

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