Journal
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
Volume 282, Issue 5, Pages L912-L916Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajplung.00303.2001
Keywords
surfactant; intracellular calcium; intercellular communication; gap junction; pulmonary hypertension; mechanical stretch; LysoTracker; heptanol; BAPTA-AM
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Funding
- NHLBI NIH HHS [HL-64896, HL-57556, HL-10142] Funding Source: Medline
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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 cmH(2)O 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.
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