Airway smooth muscle adapts to different lengths with functional changes that suggest plastic alterations in the filament lattice. To look for structural changes that might be associated with this plasticity, we studied the relationship between isometric force generation and myosin thick filament density in cell cross sections, measured by electron microscope, after length oscillations applied to the relaxed porcine trachealis muscle. Muscles were stimulated regularly for 12 s every 5 min. Between two stimulations, the muscles were submitted to repeated passive +/- 30% length changes. This caused tetanic force and thick-filament density to fall by 21 and 27%, respectively. However, in subsequent tetani, both force and filament density recovered to preoscillation levels. These findings indicate that thick filaments in airway smooth muscle are labile, depolymerization of the myosin filaments can be induced by mechanical strain, and repolymerization of the thick filaments underlies force recovery after the oscillation. This thick-filament lability would greatly facilitate plastic changes of lattice length and explain why airway smooth muscle is able to function over a large length range.

Airway smooth muscle is able to adapt and maintain a nearly constant maximal force generation over a large length range. This implies that a fixed filament lattice such as that found in striated muscle may not exist in this tissue and that plastic remodeling of its contractile and cytoskeletal filaments may be involved in the process of length adaptation that optimizes contractile filament overlap. Here, we show that isometric force produced by airway smooth muscle is independent of muscle length over a twofold length change; cell cross-sectional area was inversely proportional to cell length, implying that the cell volume was conserved at different lengths; shortening velocity and myosin filament density varied similarly to length change: increased by 69.4% Ϯ 5.7 (SE) and 76.0% Ϯ 9.8, respectively, for a 100% increase in cell length. Muscle power output, ATPase rate, and myosin filament density also have the same dependence on muscle cell length: increased by 35.4% Ϯ 6.7, 34.6% Ϯ 3.4, and 35.6% Ϯ 10.6, respectively, for a 50% increase in cell length. The data can be explained by a model in which additional contractile units containing myosin filaments are formed and placed in series with existing contractile units when the muscle is adapted at a longer length. muscle contraction; myosin filaments; ATPase activity; electron microscopy RECENT STUDIES HAVE DEMONSTRATED that the cycle of contraction and relaxation in airway smooth muscle involves polymerization and depolymerization of the actin (9, 13) and myosin (6) filaments. This lability of contractile filaments during muscle activation resembles that of nonmuscle motile cells that rely on impromptu assembly of contractile apparatus for motility. Oscillatory strains applied to single airway smooth muscle cells have revealed plastic deformation similar to that observed in soft glassy materials (3). Functional studies of airway smooth muscle indicate that the cells maintain maximal isometric force production (optimal contractile filament overlap) over a threefold length change by varying the number of contractile units in series (15). This newly emerged "plasticity" model of smooth muscle contraction is incompatible with the current concept of contraction based on the relatively restrictive model of striated muscle that possesses filament arrays in fixed lattice, which cannot accommodate large changes in cell length without compromising force production (4).The feasibility of the plasticity model can be tested experimentally based on the model predictions: the recruitment of additional contractile units in muscles adapted to longer lengths should result in an increase in thick filament content (or mass) in individual muscle cells, and as a consequence, the metabolic rate should increase with muscle length. In the present study, we tested the plasticity hypothesis through quantitative analysis of mechanical properties and ultrastructure, and measurement of the rate of ATP consumption in airway smooth muscles adapted to different lengths. MATERIALS AND METHODSMuscl...

Vascular smooth muscle shows both plasticity and heterogeneity with respect to Ca2+ signaling. Physiological perturbations in cytoplasmic Ca2+ concentration ([Ca2+]i) may take the form of a uniform maintained rise, a transient uniform [Ca2+]i elevation, a transient localized rise in [Ca2+]i (also known as spark and puff), a transient propagated wave of localized [Ca2+]i elevation (Ca2+ wave), recurring asynchronous Ca2+ waves, or recurring synchronized Ca2+ waves dependent on the type of blood vessel and the nature of stimulation. In this overview, evidence is presented which demonstrates that interactions of ion transporters located in the membranes of the cell, sarcoplasmic reticulum, and mitochondria form the basis of this plasticity of Ca2+signaling. We focus in particular on how the junctional complexes of plasmalemma and superficial sarcoplasmic reticulum, through the generation of local cytoplasmic Ca2+ gradients, maintain [Ca2+]i oscillations, couple these to either contraction or relaxation, and promote Ca2+ cycling during homeostasis.