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1 Division of Pharmaceutical Sciences, University of Wyoming College of Health Sciences, Laramie, WY, USA
2 Department of Pharmacology, Physiology and Therapeutics, University of North Dakota School of Medicine, Grand Forks, ND, USA
3 Grand Forks Human Nutrition Research Center, United States Department of Agriculture, Grand Forks, ND, USA
4 Center for Biomedical Research, University of North Dakota School of Medicine, Grand Forks, ND, USA
* To whom correspondence should be addressed. E-mail: jren{at}uwyo.edu.
Women with functional ovaries have a lower cardiovascular risk than age-matched men and postmenopausal women. However, estrogen replacement therapy remains ontroversial. The present study was designed to examine the effect of ovarian hormone deficiency and estrogen replacement on ventricular myocyte contractile function and protein kinase B (PKB)/Akt activation. Mature nulliparous female rats were subjected to bilateral ovariectomy (Ovx) or sham-operation (Sham). A subgroup of Ovx rats received estrogen (E2) replacement (40 µg/kg/d, i.p.) for 8 weeks. Mechanical and intracellular Ca2+ properties were evaluated in ventricular myocytes including peak shortening (PS), time-to-PS (TPS), time-to-90% relengthening (TR90), maximal velocity of shortening/relengthening (±dL/dt), intracellular Ca2+ fura-2 fluorescence intensity (FFI) and decay rate (
). Levels of sarco(endo)plasmic reticulum Ca,2+-ATPase (SERCA2a), phospholamban (PLB) and PKB/Akt were assessed by Western blot. Ovx promoted body weight gain associated with significantly reduced serum E2 level and uterine weight, all of which were abolished by E2 replacement. Ovx depressed PS and ±dL/dt, prolonged TPS, TR90 and , and enhanced resting FFI, all of which, with the exception of TPS, were restored by E2 replacement. Ovx did not significantly alter the levels of SERCA2a, PLB and total Akt, but did significantly reduce Akt activation (pAkt), pAkt/Akt ratio and SERCA2a/PLB ratio. These alterations in protein expression were again restored by E2 replacement. E2 enhanced PS and + dL/dt in vitro, which was abolished by the E2 receptor antagonist ICI182,780. In addition, Ovx reduced the myocyte responsiveness to increased extracellular Ca2+ and lessened increased stimulating frequency-induced decline in PS, both ablated by E2 replacement. These data suggest that both mechanical and protein functions of ventricular myocytes are directly regulated by the presence of the ovarian hormone estrogen.
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