Hypocapnia-induced contraction of porcine airway smooth muscle

Abstract

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.