Abstract
Vascular reactivity changes dramatically during postnatal maturation due in large part to developmetal changes in myofilament calcium sensitivity. In turn, our recent findings suggest that reactivity of the thick filament component of calcium sensitivity, which is measured as the relation between cytosolic calcium concentration and the extent of myosin light chain (MLC) phosphorylation, is upregulated in fetal compared to adult arteries. The present study tests the hypothesis that upregulation of fetal thick filament reactivity is due to upregulation of myosin light chain kinase (MLCK) activity. Western blot analysis revealed that MLCK abundance was 6.5±0.4 fold greater in adult than in fetal arteries. Total MLCK activity, estimated as the rate of phosphorylation of the substrate myosin light chain in intact arteries, was greater in fetal (7.9 ± 0.3 %/sec) than in adult (6.6 ± 0.3 %/sec) preparations. When total MLCK activity was normalized relative to MLCK abundance to estimate the specific activity of MLCK (%phosphorylation/sec/μg MLCK), these estimates were dramatically greater in fetal (45.5 ± 2.3) than in adult (5.8 ± 0.5) arteries. Together, these results indicate that upregulation of MLCK specific activity contributes significantly to upregulation of thick‐filament reactivity in fetal compared to adult ovine carotid arteries. Supported by NIH HD31226, HL54120, and HL64867.
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