Cellular mechanism of muscle contraction of bronchial smooth muscle

Abstract

Airway smooth muscle is one of the main effector of bronchial reactivity. The 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. The 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 the cytosolic calcium (Ca2+i) via activation of calcium channels which depend on surface membrane potential changes (electromechanical coupling) on the one hand and mainly via mechanisms independent of surface membrane potential changes-so-called the pharmacomechanical coupling--which involves membrane phosphoinositides 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. Experimental techniques that enable to simultaneously study different aspects of the cellular response are being developed in airway smooth muscle and are likely to provide complementary information about the cellular physiology and pathophysiology of this muscle.