Hypocapnia constricts peripheral airways in vivo. This study investigated the role of airway smooth muscle in this phenomenon and the mechanism of hypocapnia-induced contraction in vitro. Isometric tension, intracellular pH (pH(i)) and intracellular free calcium concentration ([Ca2+](i)) were measured in porcine airway smooth muscles suspended in organ baths in the presence of 5% or 0% CO2. In tracheal strips precontracted with carbachol, hypocapnic challenge (0% CO2) produced increases in tension, pH(i), and [Ca2+](i). In bronchial rings or tracheal strips precontracted with carbachol, nifedipine administered between consecutive contractions attenuated responses to hypocapnia (75 ± 11% above carbachol-precontracted tension before nifedipine versus 39 ± 9% after nifedipine, n = 7 bronchial rings, p < .05). Neither indomethacin (5 μM), nordihydroguaiaretic acid (10 μM) nor phenidone (10 μM) significantly altered responses. These data suggest that enhanced Ca2+ influx through voltage-dependent Ca2+ channels of airway smooth muscle cells important in airways responses to hypocapnia.
- 27',7'-bis(2-carboxyethyl)-5(6)- carboxyfluorescein
- Airway smooth muscle
- Calcium channels
- Intracellular free calcium ions
- Intracellular pH
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine