title: Force augmentation and stimulated actin polymerization in swine carotid artery.
abstract: The phenomenon of posttetanic potentiation, in which a single submaximal contraction or series of submaximal contractions strengthens a subsequent contraction, has been observed in both skeletal and cardiac muscle. In this study, we describe a similar phenomenon in swine carotid arterial smooth muscle. We find that a submaximal K(+) depolarization increases the force generation of a subsequent maximal K(+) depolarization; we term this "force augmentation." Force augmentation was not associated with a significant increase in crossbridge phosphorylation or shortening velocity during the maximal K(+) depolarization, suggesting that the augmented force was not caused by higher crossbridge phosphorylation or crossbridge cycling rates. We found that the characteristics of the tissue before the maximal K(+) depolarization predicted the degree of force augmentation. Specifically, measures of stimulated actin polymerization (higher prior Y118 paxillin phosphorylation, higher prior F-actin, and transition to a more solid rheology evidenced by lower noise temperature, hysteresivity, and phase angle) predicted the subsequent force augmentation. Increased prior contraction alone did not induce force augmentation since readdition of Ca(2+) to Ca(2+)-depleted tissues induced a partial contraction that was not associated with changes in noise temperature or with subsequent force augmentation. These data suggest that stimulated actin polymerization may produce a substrate for increased crossbridge mediated force, a process we observe as force augmentation.
authors.affiliation: Cardiovascular Division, Univ. of Virginia Health System, Charlottesville, VA 22908-0146, USA.
authors.forename: Ankit D
authors.initials: AD
authors.lastname: Tejani
authors.forename: Christopher M
authors.initials: CM
authors.lastname: Rembold
mesh_terms: D000199:Actins / Q000502:physiology*; D000818:Animals; D002118:Calcium / Q000494:pharmacology; D017536:Carotid Artery, Common / Q000187:drug effects / Q000502:physiology*; D007700:Kinetics; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology; D051419:Paxillin / Q000378:metabolism / Q000494:pharmacology; D010766:Phosphorylation; D011188:Potassium / Q000502:physiology; D013314:Stress, Mechanical; D013552:Swine; D013742:Tetanus
chemical_list: D000199:Actins; D051419:Paxillin; D011188:Potassium; D002118:Calcium