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Research Article

Force augmentation and stimulated actin polymerization in swine carotid artery

¹University of Virginia

Submitted 21 July 2009 ; revised 31 August 2009 ; accepted in final form 25 September 2009

The phenomenon of post-tetanic 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 prior to 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 Ca²⁺ to Ca²⁺-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.

actin; noise temperature; paxillin; vascular smooth muscle