Evidence for Absence of Latch-Bridge Formation in Muscular Saphenous Arteries

Document Type

Article

Language

eng

Format of Original

9 p.

Publication Date

7-2006

Publisher

American Physiological Society

Source Publication

American Journal of Physiology - Heart and Circulatory Physiology

Source ISSN

1562-4129

Original Item ID

DOI: 10.1152/ajpheart.00977.2005

Abstract

Large-diameter elastic arteries can produce strong contractions indefinitely at a high-energy economy by the formation of latch bridges. Whether ownstream blood vessels also use latch bridges remains unknown. The zero-pressure medial thickness and lumen diameter of rabbit saphenous artery (SA), a muscular branch of the elastic femoral artery (FA), were, respectively, approximately twofold and half-fold that of the FA. In isolated FA and SA rings, KCl rapidly (s) caused strong increases in isometric stress (1.2 x 105 N/m2) and intracellular Ca2+ concentration ([Ca2+]i; 250 nM). By 10 min, [Ca2+]i declined to ~175 nM in both tissues, but stress was sustained in FA (1.3 x 105 N/m2) and reduced by 40% in SA (0.8 x 105 N/m2). Reduced tonic stress correlated with reduced myosin light chain (MLC) phosphorylation in SA (28 vs. 42% in FA), and simulations with the use of the four-state kinetic latch-bridge model supported the hypothesis that latch-bridge formation in FA, but not SA, permitted maintenance of high stress values at steady state. SA expressed more MLC phosphatase than FA, and permeabilized SA relaxed more rapidly than FA, suggesting that MLC phosphatase activity was greater in SA than in FA. The ratio of fast-to-slow myosin isoforms was greater for SA than FA, and on quick release, SA redeveloped isometric force faster than FA. These data support the hypothesis that maintained isometric force was 40% less in SA than in FA because expressed motor proteins in SA do not support latch-bridge formation.

Comments

American Journal of Physiology - Heart and Circulatory Physiology, Vol. 291 (July 2006). DOI.

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