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Department of Physiology, University of Adelaide, Adelaide, South Australia, 5005, Australia
Pulmonary
surfactant, a mixture consisting of lipids and proteins and secreted 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
sympathetic nervous system and changes in ventilatory pattern. The
parasympathetic nervous system is not believed to affect surfactant
secretion in mammals. Very little is known about the factors that
control surfactant secretion in nonmammalian vertebrates. Here, a new
methodology for the isolation and culture 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 cholesterol (Chol)
secretion. At 37°C, only Epi stimulated
secretion of total PL and DSP from primary cultures of lizard type II
cells, and secretion was blocked by the
-adrenoreceptor antagonist
propranolol. Neither of the agonists affected Chol secretion. At
18°C, Epi and ACh both stimulated DSP and PL secretion but not Chol
secretion. The secretion of surfactant Chol does not appear to be under
autonomic control. It appears that the secretion of surfactant PL is
predominantly controlled by the autonomic nervous system in lizards.
The sympathetic nervous system may control surfactant secretion at high
temperatures, whereas the parasympathetic nervous system may
predominate at lower body temperatures, stimulating surfactant
secretion without elevating metabolic rate.
adrenergic agonist; cholinergic agonist; phospholipids; cholesterol; temperature
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