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Articles in PresS, published online ahead of print July 11, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00281.2002
Submitted on April 1, 2002
Accepted on June 28, 2002
1 Molecular Pharmacology, Physiology & Biotechnology, Brown University, Providence, RI, USA
2 Pediatrics, Women and Infants' Hospital of Rhode Island, Providence, RI, USA
* To whom correspondence should be addressed. E-mail: chi-ming_hai{at}brown.edu.
We tested the hypothesis that maternal antenatal glucocorticoid treatment modulates 17 kD myosin light chain (LC17) isoform expression and the contractile time course in fetal ovine carotid arteries. In response to 1 µM phenylephrine, arteries from fetuses of dexamethasone treated ewes exhibited biphasic contractions, characterized by an intermediate relaxation phase between initial force development and steady-state force maintenance. The rate constant of the relaxation phase was significantly higher in the arteries from the fetuses of the dexamethasone than placebo treated ewes. The observed biphasic contractions suggest the appearance of functional sarcoplasmic reticulum in the arteries from the fetuses of the dexamethasone treated ewes. The myosin LC17a isoform expression was lower in the arteries from the fetuses of the placebo treated ewes than in those from the ewes. Repeated maternal administration of dexamethasone induced an almost two-fold increase in myosin LC17a isoform expression in the fetal arteries. In contrast, myosin LC17a isoform expression in maternal carotid arteries was not affected by dexamethasone treatment. These observations indicate that dexamethasone accelerates the development of myosin LC17a isoform expression in fetal arteries, but not in adult arteries. We speculate that the dexamethasone-related increases in myosin LC17a isoform expression in fetal arteries represent accelerated differentiation of a subpopulation of vascular smooth muscle cells from the fetal to the adult phenotype.
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