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This Article Full Text Full Text (PDF) All Versions of this Article: 288/1/H142    most recent 00655.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (5) Citing Articles via Google Scholar Google Scholar Articles by Xiao, D. Articles by Zhang, L. Search for Related Content PubMed PubMed Citation Articles by Xiao, D. Articles by Zhang, L.

Adaptation of uterine artery thick- and thin-filament regulatory pathways to pregnancy

Center for Perinatal Biology, Department of Physiology and Pharmacology, School of Medicine, Loma Linda University, Loma Linda, California

Submitted 2 July 2004 ; accepted in final form 18 August 2004

Little is known about the adaptation of uterine artery smooth muscle contractile mechanisms to pregnancy. The present study tested the hypothesis that pregnancy differentially regulates thick- and thin-filament regulatory pathways in uterine arteries. Isometric tension, intracellular free Ca²⁺ concentration, and phosphorylation of 20-kDa myosin light chain (MLC₂₀) were measured simultaneously in uterine arteries isolated from nonpregnant and near-term (140 days gestation) pregnant sheep. Phenylephrine-mediated intracellular free Ca²⁺ concentration, MLC₂₀ phosphorylation, and contraction tension were significantly increased in uterine arteries of pregnant compared with nonpregnant animals. In contrast, phenylephrine-mediated Ca²⁺ sensitivity of MLC₂₀ phosphorylation was decreased in the uterine arteries of pregnant sheep. Simultaneous measurement of phenylephrine-stimulated tension and MLC₂₀ phosphorylation in the same tissue indicated a decrease in MLC₂₀ phosphorylation-independent contractions in the uterine arteries of pregnant sheep. In addition, activation of PKC produced significantly lower sustained contractions in uterine arteries of pregnant compared with nonpregnant animals in the absence of changes in MLC₂₀ phosphorylation levels in either vessels. In uterine arteries of nonpregnant sheep, the mitogen-activated protein kinase kinase/extracellular signal-regulated kinase inhibitor PD-098059 significantly increased phenylephrine-mediated, MLC₂₀ phosphorylation-independent contractions. The results suggest that in uterine arteries, pregnancy upregulates ₁-adrenoceptor-mediated Ca²⁺ mobilization and MLC₂₀ phosphorylation. In contrast, pregnancy downregulates the Ca²⁺ sensitivity of myofilaments, which is mediated by both thick- and thin-filament pathways.

₁-adrenoceptor; protein kinase C; calcium; myosin light chain phosphorylation; extracellular signal regulated kinase

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