Mechanisms Involved in the Mediation of Contractions of Airway Smooth Muscle to Arachidonate Metabolites and Other Spasmogens
Airway smooth muscle (ASM) contractility, like that of other smooth muscle types, is dependent on the level of free intracellular Ca2+, which is precisely regulated by the supply of ionized Ca2+ made available from intra- and extracellular pools (Filo et al., 1965; Solmyo and Solmyo, 1968; Bolton, 1979). Membrane-potential-dependent and -independent mechanisms are involved in Ca2+ regulation in response to receptor stimulation by a variety of neural, humoral, and myogenic stimuli (Kirkpatrick et al., 1975; Coburn and Yamaguchi, 1977; Farley and Miles, 1977; Bolton, 1979). These collectively serve to control smooth muscle contractility and also may influence the underlying state of tissue reactivity. Of particular importance in lung physiology and pathophysiology are the potent bronchoactive substances, namely, prostaglandins, endoperoxides, thromboxanes (Samuelsson et al., 1978), and, more recently, leukotrienes (Samuelsson et al., 1981). The exquisite sensitivity of respiratory tissue to eicosanoids and in particular the sulfidoleukotrienes is well recognized (Hedquist et al., 1980; Drazen et al., 1980; Piper et al., 1981; Jones et al., 1982a). However, little information is available on their precise mechanism of action, their receptors, or the specific Ca2+ pools required for full expression of their biological activity in the lung.
KeywordsAirway Smooth Muscle Contractile Response Contractile Activity Entry Blocker Tracheal Smooth Muscle
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