Control of pulmonary surfactant secretion from type II pneumocytes isolated from the lizard Pogona vitticeps

Pulmonary surfactant, a mixture consisting of lipids and proteins and secre ted by type II cells, functions to reduce the surface tension of the fluid lining of the lung, and thereby decreases the work of breathing. In mammals , surfactant secretion appears to be influenced primarily by the sympatheti c nervous system and changes in ventilatory pattern. The parasympathetic ne rvous system is not believed to affect surfactant secretion in mammals. Ver y little is known about the factors that control surfactant secretion in no nmammalian vertebrates. Here, a new methodology for the isolation and cultu re of type II pneumocytes from the lizard Pogona vitticeps is presented. We examined the effects of the major autonomic neurotransmitters, epinephrine (Epi) and ACh, on total phospholipid (PL), disaturated PL (DSP), and chole sterol (Chol) secretion. At 37 degrees C, only Epi stimulated secretion of total PL and DSP from primary cultures of lizard type IT cells, and secreti on was blocked by the P-adrenoreceptor antagonist propranolol. Neither of t he agonists affected Chol secretion. At 18 degrees C, Epi and ACh both stim ulated DSP and PL secretion but not Chol secretion. The secretion of surfac tant Chol does not appear to be under autonomic control. It appears that th e secretion of surfactant PL is predominantly controlled by the autonomic n ervous system in lizards. The sympathetic nervous system may control surfac tant secretion at high temperatures, whereas the parasympathetic nervous sy stem may predominate at lower body temperatures, stimulating surfactant sec retion without elevating metabolic rate.