title: Cross-bridge dephosphorylation and relaxation of vascular smooth muscle.
abstract: 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.
authors.affiliation: Department of Physiology, School of Medicine, University of Virginia, Charlottesville 22908.
authors.forename: C M
authors.initials: CM
authors.lastname: Hai
authors.forename: R A
authors.initials: RA
authors.lastname: Murphy
mesh_terms: D000818:Animals; D002339:Carotid Arteries / Q000187:drug effects / Q000502:physiology; D004558:Electric Stimulation; D066298:In Vitro Techniques; D007537:Isometric Contraction / Q000187:drug effects; D007700:Kinetics; D009119:Muscle Contraction / Q000187:drug effects; D009126:Muscle Relaxation / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology*; D015879:Myosin Subfragments; D009218:Myosins / Q000502:physiology*; D009543:Nifedipine / Q000494:pharmacology; D010446:Peptide Fragments / Q000502:physiology*; D010766:Phosphorylation; D013552:Swine; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology
chemical_list: D015879:Myosin Subfragments; D010446:Peptide Fragments; D013757:Tetraethylammonium Compounds; D019789:Tetraethylammonium; D009218:Myosins; D009543:Nifedipine