RELAXATION OF SMOOTH-MUSCLE

We have demonstrated that in dogs antigen sensitization results in alt erations of contractile properties. These changes could account for th e hyperresponsiveness reported in asthma. The failure of the muscle to relax could be another important factor responsible for maintaining h igh airway resistance. We therefore developed an index of isotonic rel axation, t(1/2,CE) (half time for relaxation that is independent of mu scle load and initial contractile element length), for evaluation of t he relaxation process. Because the maximum shortening velocity at 2 s but not at 10 s was greater in sensitized bronchial smooth muscle than that in controls, studies of relaxation were also undertaken at these two times. The mean half-relaxation time indicated by t(1/2,CE) showe d no difference between sensitized and control muscles after 10 s of s timulation (8.38 +/- 0.92 vs. 7.78 +/- 0.93 s, means +/- SE); however, it was prolonged significantly in the sensitized muscle only stimulat ed for 1 s (12.74 +/- 2.5 s, mean +/- SE) compared with the control (6 .98 +/- 1.01 s). During the late phase of isotonic relaxation, both gr oups showed an unexpected spontaneous increase in zero-load shortening velocity, which is an index of cross-bridge cycling rate. We conclude that (i) both contraction and relaxation properties of early normally cycling cross bridges are altered after sensitization and these chang es may account for the hyperresponsiveness observed in asthmatics and (ii) the cross-bridge cycling rate increases spontaneously during isot onic relaxation, probably as a result of reactivation of the contracti le mechanism.