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The present study tests the hypothesis that age-related differences in contractility of cerebral arteries from hypoxic animals involve changes in myofilament Ca 2+ sensitivity. Basilar arteries from term fetal and nonpregnant adult sheep maintained 110 days at 3,820 m were used in measurements of cytosolic calcium concentration (Ca 2+ i ), myosin light chain phosphorylation, and contractile tensions induced by graded concentrations of K + or serotonin (5-HT). Slopes relating Ca 2+ i to tension were similar in fetal (0.83 ± 0.07) and adult (1.02 ± 0.08) arteries for K + contractions but were significantly greater for fetal (3.77 ± 0.64) than adult (2.00 ± 0.13) arteries for 5-HT contractions. For both K + and 5-HT contractions, these relations were left shifted in fetal compared with adult arteries, indicating greater Ca 2+ sensitivity in fetal arteries. In contrast, slopes relating Ca 2+ i and %myosin phosphorylation for K + contractions were less in fetal (0.37 ± 0.08) than adult (0.81 ± 0.07) arteries, and the fetal curves were right shifted. For 5-HT contractions, the slope of the Ca 2+ -phosphorylation relation was similar in fetal (0.33 ± 0.09) and adult (0.33 ± 0.23) arteries, indicating that 5-HT depressed Ca 2+ -induced myosin phosphorylation in adult arteries. For slopes relating %myosin phosphorylation and tension, fetal values (K + : 1.52 ± 0.22, 5-HT: 7.66 ± 1.70) were less than adult values (K + : 2.13 ± 0.30, 5-HT: 8.29 ± 2.40) for both K + - and 5-HT-induced contractions, although again fetal curves were left shifted relative to the adult. Thus, in hypoxia-acclimatized basilar arteries, a downregulated ability of Ca 2+ to promote myosin phosphorylation is offset by an upregulated ability of phosphorylated myosin to produce force yielding an increased fetal myofilament Ca 2+ sensitivity. Postnatal maturation reprioritizes the mechanisms regulating hypoxic contractility through changes in the source of activator Ca 2+ , the pathways governing myosin light chain phosphorylation, and its interaction with actin. cerebral arteries; myofilament calcium sensitivity; postnatal maturation; myosin phosphorylation; thin filament regulation Address for reprint requests and other correspondence: W. J. Pearce, Center for Perinatal Biology, Loma Linda University School of Medicine, Loma Linda, CA 92350 (E-mail: wpearce@llu.edu )
Journal of Applied Physiology – The American Physiological Society
Published: Jul 1, 2005
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