Neurogenic stimulation, cytokine and mediator release affect the system postjunctionally, as in the lower panel. These postjunctional factors potentially increase maximal airway narrowing. Smooth muscle hypertrophy and/or hyperplasia ( i ) leads to an enhanced contractile response. There is some evidence that in addition the inflammatory process in asthma is associated with increased actomyosin ATP-ase activity, leading to greater shortening velocity and greater maximal shortening.
Mediators and cytokines may be delivered to the airways via the circulatory system ( j ); they may be generated by processes outside the lung, or be locally produced and be transported down the airways by the bronchial circulation.
Adventitial swelling ( k ) increases the outer airway circumference, due to which smooth muscle contraction may be less opposed by the elastic pull from alveolar attachments. Increased airway secretions ( n ) and exudate diminish airway lumen and, together with increased airway compliance ( o ) amplify the effect of smooth muscle contraction. This may also be due to collagen deposition in the subepithelial reticular layer ( l ) associated with chronic inflammation in asthma, but then collagen might stiffen the airway. The submucosal swelling leads to diminished epithelial folding ( m ) and liquid filling of interstices between epithelial projections. The force developed by smooth muscle depends on its initial length (length-tension relationship); this is influenced by lung elastic recoil and hence lung volume ( p ), and loss of alveolar attachments ( q ). The latter factors also determine the elastic load to contracting muscles.