Fluoride (F-), a known stimulator of G-protein, induced strong contraction in rabbit trachealis muscle. AlCl<sub>3</sub>(5 ~ 20 μM), which is required for G-protein stimulation by F<sup>-</sup>, potentiated the contractile response to F<sup>-</sup>. Ca<sup>2+</sup>-removal and verapamil, a calcium channel blocker, inhibited the fluoroaluminate-induced contraction. Fluoroaluminate increased <sup>45</sup>Ca influx in the absence and presence of verapamil. In heparin-loaded muscle high K<sup>+</sup>-induced contraction was not affected, but acetylcholine and fluoroaluminate-induced contractions were inhibited. The fluoroaluminate-induced contraction was partially relaxed by isoproterenol, a stimulator of adenylate cyclase. Pertussis toxin partially inhibited fluoroaluminate-induced contraction and potentiated isoproterenol-induced relaxation in the presence of fluoroaluminate, but had no effect on acetylcholine-induced contraction and the isoproterenol-induced relaxation in the presence of acetylcholine. These results suggest that fluoroaluminate has the ability to stimulate at least two putative G-proteins in rabbit trachealis muscle; One causes Ca<sup>2+</sup> influx through the potential-operated Ca<sup>2+</sup> channel and the other induces intracellular Ca<sup>2+</sup> release by the increase of inositol-1, 4, 5-triphosphate.