Perturbed Equilibria of Myosin Binding

Perturbed Equilibria of Myosin Binding In asthma, the mechanisms relating airway obstruction, hyperresponsiveness, and inflammation remain rather mysterious. The regulation of airway smooth muscle length and an airway diameter corresponds to a dynamically equilibrated steady state that requires a continuous supply of external mechanical energy (derived from tidal lung inflations) acting to perturb the interactions of myosin with actin, drives the molecular state of the system far away from thermodynamic equilibrium, and biases the muscle toward mechanically induced relaxation. This mechanism may help to elucidate several unexplained phenomena including the multifactorial origins of airway hyperresponsiveness, how allergen sensitization leads to airway hyperresponsiveness, how hyperresponsiveness can persist long after airway inflammation is resolved, and the inability of deep inspirations to relax airway smooth muscle in asthma.