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Am J Physiol Heart Circ Physiol 283: H1743-H1749, 2002. First published July 11, 2002; doi:10.1152/ajpheart.00281.2002
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Vol. 283, Issue 5, H1743-H1749, November 2002

Maternal dexamethasone treatment alters myosin isoform expression and contractile dynamics in fetal arteries

Chi-Ming Hai1, Grazyna Sadowska2, Louise Francois1, and Barbara S. Stonestreet2

1 Department of Molecular Pharmacology, Physiology and Biotechnology and 2 Department of Pediatrics, Women and Infants' Hospital of Rhode Island, Brown University School of Medicine, Providence, Rhode Island 02912

We tested the hypothesis that maternal glucocorticoid treatment modulates 17-kDa myosin light chain (myosin LC17) isoform expression and contractile dynamics in fetal ovine carotid arteries. In the single course group, ewes received 6 mg dexamethasone or placebo over 48 h. In the repeated course group, ewes received 6 mg dexamethasone or placebo weekly for 5 wk. In response to 1 µM phenylephrine, arteries from fetuses of dexamethasone-treated ewes exhibited biphasic contractions, characterized by an intermediate relaxation phase. The relaxation rate constant was significantly higher in arteries from the fetuses of dexamethasone than placebo-treated ewes. The observed biphasic contractions suggest the appearance of functional sarcoplasmic reticulum in the arteries from the fetuses of 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 twofold increase in myosin LC17a isoform expression in the fetal arteries. In contrast, maternal myosin LC17a isoform expression was not affected by dexamethasone treatment. We speculate that dexamethasone-induced increases in fetal myosin LC17a isoform expression represent accelerated differentiation of a subpopulation of vascular smooth muscle cells from the fetal to adult phenotype.

development; glucocorticoid; hypertension; programming


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