Cross-bridge dephosphorylation and relaxation of vascular smooth muscle.

We tested the hypothesis that relaxation in vascular smooth muscle is the result of inactivation of myosin light chain kinase and cross-bridge dephosphorylation. Fast neurally mediated contractions of swine carotid medial strips were induced by electrical field stimulation. Termination of the stimulus resulted in relaxation with a half time of 2 min. Nifedipine (0.1 microM) increased the relaxation rate without significant effects on the contractile response. Cross-bridge dephosphorylation was much faster than stress decay with basal levels reached within 1 min when 73% of the developed stress remained. The time-course data of dephosphorylation and stress were analyzed with a model that predicted the dependences of stress and isotonic shortening velocity on cross-bridge phosphorylation during contraction. Rate constants resolved from contraction data also fitted the relaxation data when the model's prediction was corrected for estimated errors in the phosphorylation measurements. Because Ca2+-dependent cross-bridge phosphorylation was the only postulated regulatory mechanism in the model, these results are consistent with the hypothesis that cross-bridge dephosphorylation is necessary and sufficient to explain relaxation in the swine carotid media.