Surfactant - Tissue Functioning and Remodeling in the Circulatory and Ventilatory Systems - page 789

13.2.2.2 Ion Carriers of Type-2 Pneumocyte

Alveolar type-2 cells (size m) cover 2 to 5% of the alveolar surface area. They

produce, secrete, and recycle alveolar surfactant. They also participate in active
ion transport, as they have Na + -K + ATPases, K + and epithelial Na + channels,
and cystic fibrosis transmembrane conductance regulators [ 1604 ]. However, they
contain fewer Na + channels than alveolar type-1 cells, at least in rodents.

∼ 10

13.2.2.3 Adenosine Receptors and Ion Transport

Adenosine operates via G-protein-coupled receptors to activate or inhibit adenylate
cyclases. Messenger cAMP regulates active Na + transport in alveolar epithelium.
Adenosine hence regulates alveolar ion transport via elevated activity of ENaC and
CFTR and airspace fluid content (para- and autocrine regulation of the alveolar fluid
clearance). At least in rodents, type-1 and -2 alveolar epithelial cells possess all
4 types of adenosine receptors (A 1 ,A 2 A ,A 2 B ,andA 3 )[ 1605 ]. Receptors A 1 and A 3
inhibit adenylate cyclase and signal via inositol 3-phosphate and phospholipase-C.
Type-2 adenosine receptor activates adenylate cyclase via G α s subunit. Recep-

tor A 2 A is expressed 5- to 9-fold more than the 3 other types in alveolar cells.
At low doses, adenosine increases alveolar fluid clearance owing to A 2 A and
A 3 receptors. At physiological doses (micromolar), adenosine reduces alveolar
fluid clearance via A 1 receptor that causes Cl − efflux through CFTR, which
counterbalances active Na + absorption.

13.2.3 Secretion and Role of Alveolar Surfactant

The surfactant that covers the alveolar wetted surface is a phospholipid, mainly
lecithin and dipalmitoyl lecithin. Lecithin consists in a long chain of fatty acids
bound to glycerol and to electrically charged phosphate and choline groups that are
attracted by polar water molecules. Pure oxygen and atmospheric pollutants affect
the alveolar surface.
The surfactant production is controlled by the vagus nerve. A decline in
surfactant activity indeed results from a cut in vagus nerve. Therefore, the release of
surfactant depends on the local blood flow to match ventilation to perfusion.
The surfactant is secreted by the type-2 granular pneumocytes of the alveolar
wall. It induces variable surface tension according to the lung volume, i.e., the
degree of alveolar expansion. It contributes to the alveolar stability, preserving the
alveoli from full collapse during expiration and hyperinflation during inspiration.
Alveoli expand more easily due to the presence of surfactant. This surface-active
agent also varies the surface tension with changes in the alveolus surface area. The
surfactant layer becomes thinner in inflated alveoli, thereby increasing the surface