Hypocapnia-induced contraction of porcine airway smooth muscle

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.