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1 Division of Pharmaceutical Sciences, University of Wyoming College of Health Sciences, Laramie, Wyoming 82071-3375; 2 University of North Dakota School of Medicine, Grand Forks 58203; 3 United States Department of Agriculture, Grand Forks Human Nutrition Research Center, Agricultural Research Service, Grand Forks 58202; and 4 Center for Biomedical Research, University of North Dakota School of Medicine, Grand Forks, North Dakota 58203
Women with functional
ovaries have a lower cardiovascular risk than men and postmenopausal
women. However, estrogen replacement therapy remains controversial.
This study examined the effect of ovarian hormone deficiency and
estrogen replacement on ventricular myocyte contractile function and
PKB/Akt activation. 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
1 · day1)
for 8 weeks. Mechanical and intracellular Ca2+ properties
were evaluated including peak shortening (PS), time to PS (TPS), time
to 90% relengthening (TR90), maximal velocity of
shortening/relengthening (±dL/dt), fura 2 fluorescence intensity (FFI), and decay rate. Levels of
sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA2a),
phospholamban (PLB), and Akt were assessed by Western blot. Ovx
promoted body weight gain associated with reduced serum E2
and uterine weight, all of which were abolished by E2. Ovx
depressed PS and ±dL/dt, prolonged TPS,
TR90, and decay rate, and enhanced resting FFI, all of
which, with the exception of TPS, were restored by E2. Ovx
did not alter the levels of SERCA2a, PLB, and total Akt, but
significantly reduced Akt activation [phosphorylated Akt (pAkt)],
pAkt/Akt, and the SERCA2a-to-PLB ratio. These alterations in protein
expression were restored by E2. E2 enhanced PS
and +dL/dt in vitro, which was abolished by the
E2 receptor antagonist ICI-182780. Ovx reduced myocyte
Ca2+ responsiveness and lessened stimulating
frequency-induced decline in PS, both ablated by E2. These
data suggest that mechanical and protein functions of ventricular
myocytes are directly regulated by E2.
ovariectomy; cardiac myocyte; contraction, intracellular Ca2+
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