Evidence for absence of latch-bridge formation in muscular saphenous arteries
- 1 July 2006
- journal article
- research article
- Published by American Physiological Society in American Journal of Physiology-Heart and Circulatory Physiology
- Vol. 291 (1), H138-H146
- https://doi.org/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 downstream 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 (5N/m2) and intracellular Ca2+concentration ([Ca2+]i; 250 nM). By 10 min, [Ca2+]ideclined to ∼175 nM in both tissues, but stress was sustained in FA (1.3 × 105N/m2) and reduced by 40% in SA (0.8 × 105N/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.Keywords
This publication has 43 references indexed in Scilit:
- An expanded latch-bridge model of protein kinase C-mediated smooth muscle contractionJournal of Applied Physiology, 2005
- Smooth muscle myosin: regulation and propertiesPhilosophical Transactions Of The Royal Society B-Biological Sciences, 2004
- Some precautions in using chelators to buffer metals in biological solutionsCell Calcium, 2004
- RhoA kinase and protein kinase C participate in regulation of rabbit stomach fundus smooth muscle contractionBritish Journal of Pharmacology, 2002
- Cyclic GMP Causes Ca2+ Desensitization in Vascular Smooth Muscle by Activating the Myosin Light Chain PhosphatasePublished by Elsevier BV ,1997
- A novel mechanism for the Ca(2+)-sensitizing effect of protein kinase C on vascular smooth muscle: inhibition of myosin light chain phosphatase.The Journal of general physiology, 1994
- Expression of four myosin heavy chain isoforms with development in mouse uterusCell Motility, 1993
- Myosin Phosphorylation and the Cross-Bridge Cycle in Arterial Smooth MuscleScience, 1981
- Architecture of the Vessel WallPublished by Wiley ,1980
- A relationship between Ca2+ sensitivity and phosphorylation of gizzard actomyosinBiochemical and Biophysical Research Communications, 1976