CONTRACTILITY AND MYOSIN HEAVY-CHAIN ISOFORM PATTERNS IN DEVELOPING TRACHEAL MUSCLE

Citation
Da. Roepke et al., CONTRACTILITY AND MYOSIN HEAVY-CHAIN ISOFORM PATTERNS IN DEVELOPING TRACHEAL MUSCLE, Respiration physiology, 98(1), 1994, pp. 101-110
Citations number
26
Categorie Soggetti
Respiratory System",Physiology
Journal title
ISSN journal
00345687
Volume
98
Issue
1
Year of publication
1994
Pages
101 - 110
Database
ISI
SICI code
0034-5687(1994)98:1<101:CAMHIP>2.0.ZU;2-#
Abstract
Changes in airway smooth muscle reactivity with development may be cau sed by either modification of the excitation-contraction coupling syst em or alteration of the contractile apparatus. The mechanism responsib le 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 supra-maximal electrical stimulati on, were recorded simultaneously as functions of time for tracheal smo oth 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 contractililty d uring post-neonatal development in rabbits. This conclusion is surpris ing 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-polyacryl imide gel electrophoresis for tracheal smooth muscle from male rabbits of 8 and 25 weeks of age. Unlike the reported MHC isoform shifts in t he 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 patter ns 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.