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Articles in PresS, published online ahead of print January 4, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00303.2001
Submitted on August 3, 2001
Accepted on December 14, 2001
* To whom correspondence should be addressed. E-mail: jb39{at}columbia.edu.
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 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 [Ca2+]i oscillations that abated on relief of pressure elevation. The rate of loss of LB fluorescence that reports the LB exocytosis rate, increased 4-fold after the pressure elevation and continued at the same rate even after pressure and [Ca2+]i oscillations had returned to baseline. In alveoli pre-treated with either BAPTA-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.
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