We have previously shown that arachidonic acid (AA)-induced contractions of indomethacin-pretreated guinea pig trachea and parenchyma are due to the synthesis of leukotrienes C4 and D4. The present experiments were designed to investigate the role of calcium (Ca2+) in the above. AA (66 microM)-induced contractions of trachea, but not parenchyma, were reduced in Ca2+-free Krebs-Henseleit solution ( KHS ). However the contractions of both trachea and parenchyma were abolished in Ca2+-free KHS with either lanthanum chloride (1 mM) or EDTA (300 microM). The Ca2+ antagonists, verapamil (100 microM), nitrendipine (100 microM), and TMB-8 (100 microM), reduced AA-induced contractions of both trachea and parenchyma. Re-addition of Ca2+ (2.2 mM) to trachea and parenchyma in Ca2+-free KHS in the presence of lanthanum restored the AA-induced contractions. This effect of Ca2+ was reduced by verapamil (100 microM) or nitrendipine (100 microM). LTC4-induced contractions of trachea and parenchyma were unaffected by nitrendipine (100 microM), whereas tracheal contractions were reduced in Ca2+-free KHS . Both tracheal and parenchymal contractions to LTC4 were reduced in Ca2+-free KHS in the presence of lanthanum chloride (1 mM). We conclude that superficially bound pools of Ca2+ are important in AA-induced contractions of the airways. Furthermore, nitrendipine reduces AA-induced contractions by inhibiting AA metabolism and not by inhibiting airway smooth muscle contraction induced by released leukotrienes.