Airway smooth muscle is one of the main effectors of bronchial reactivity. Our understanding of the cellular mechanisms involved in the contraction of this muscle has advanced in the recent past since isolated cells in culture can now be studied. Extracellular messengers (neurotransmitters and mediators) as well as their specific membrane receptors have been analyzed in some details. Membrane transduction of extracellular messengers brings about the formation (or the increase in the concentration) of the intracellular second messenger which, in airway smooth muscle, is cytosolic calcium (Ca2+i) via activation of calcium channels which depend on surface membrane potential changes (electromechanical coupling) on one hand and mainly via mechanisms independent of surface membrane potential changes, the so called--pharmacomechanical coupling--which involves membrane phosphoinositide metabolism. Changes in Ca2+i activate contractile proteins leading the muscle to shorten and to develop force via several controlled steps such as phosphorylation of myosin or changes in the sensitivity to Ca2+ of the contractile elements. Information about the cellular physiology and pathophysiology of this muscle is of value to design new drugs for the treatment of bronchoconstriction.