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Am J Physiol Lung Cell Mol Physiol 282: L912-L916, 2002. First published January 4, 2002; doi:10.1152/ajplung.00303.2001
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Vol. 282, Issue 5, L912-L916, May 2002

SPECIAL TOPIC
Mechanotransduction in the Lung
Vascular regulation of type II cell exocytosis

P. M. Wang, E. Fujita, and J. Bhattacharya

Departments of Medicine and Physiology and Cellular Biophysics, College of Physicians and Surgeons; and St. Luke's-Roosevelt Hospital Center, Columbia University, New York, New York 10019

To determine whether lung capillary pressure regulates surfactant secretion, we viewed alveoli of the constantly inflated, isolated blood-perfused rat lung by fluorescence microscopy. By alveolar micropuncture we infused fura 2 and lamellar body (LB)-localizing dyes for fluorescence detection of, respectively, the alveolar cytosolic Ca2+ concentration ([Ca2+]i) and type II cell exocytosis. Increasing left atrial pressure (Pla) from 5 to 10 cmH2O increased septal capillary diameter by 26% and induced marked alveolar [Ca2+]i oscillations that abated on relief of pressure elevation. The rate of loss of LB fluorescence that reflects the LB exocytosis rate increased fourfold after the pressure elevation and continued at the same rate even after pressure and [Ca2+]i oscillations had returned to baseline. In alveoli pretreated with either 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-AM, the intracellular Ca2+ chelator, or heptanol, the gap junctional blocker, the pressure-induced exocytosis was completely inhibited. We conclude that capillary pressure and surfactant secretion are mechanically coupled. The secretion initiates in a Ca2+-dependent manner but is sustained by Ca2+-independent mechanisms.

surfactant; intracellular calcium; intercellular communication; gap junction; pulmonary hypertension; mechanical stretch; LysoTracker; heptanol; BAPTA-AM


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