Contractility and myosin heavy chain isoform patterns in developing tracheal muscle

Changes in airway smooth muscle reactivity with development may be caused by either modification of the excitation-contraction coupling system or alteration of the contractile apparatus. The mechanism responsible for the reported changes in reactivity was addressed in this study by examining airway smooth muscle contractility and myosin heavy chain isoform patterns as a function of post-neonatal development. Changes in length and force, in response to supramaximal electrical stimulation, were recorded simultaneously as functions of time for tracheal smooth muscle (TSM) strips from 8-week-old and 25-week-old male rabbits. Both the passive and active length-tension (L-T) curves as well as the force-velocity (F-V) curves for the two age groups of rabbit TSM were not significantly different indicating no changes in contractility during post-neonatal development in rabbits. This conclusion is surprising in light of reports of myosin heavy chain (MHC) isoform shifts in porcine trachealis during comparable periods of development. Therefore, MHC isoform ratios were compared by sodium dodecyl sulfate-polyacrylimide gel electrophoresis for tracheal smooth muscle from male rabbits of 8 and 25 weeks of age. Unlike the reported MHC isoform shifts in the pig tracheal muscle, the rabbit trachealis showed no difference in MHC isoform ratios between the two age groups compared in this study. In conclusion, no changes occur in contractility or MHC isoform patterns during post-neonatal development of rabbit tracheal smooth muscle. Therefore, reported changes in airway muscle reactivity are likely due to changes in receptors or in second messenger systems rather than to changes in the contractile apparatus.