Abstract
In this issue of Hypertension , Jazbutyte et al1 introduce the novel idea that aging impairs the ability of the heart to respond to estrogen replacement. Using young (3-month-old) and senescent (24-month-old) spontaneously hypertensive rats (SHRs), they compared the effect of estrogen on cardiac hypertrophy and gene expression in rats given ovariectomy with and without estrogen replacement. They hypothesized that estrogen replacement would differentially alter the cardiac hypertrophic response to ovariectomy. After sham or ovariectomy surgery with and without estrogen replacement, the young and senescent rats were followed for 6 weeks. Blood pressure was elevated in all of the groups and was not affected by estrogen supplementation. Estrogen attenuated the increase in relative heart weight in the ovariectomized young group but not in the senescent group. Cardiac estrogen receptor α levels were lower in the senescent rats (both intact and ovariectomy groups) compared with the corresponding young groups, and estrogen replacement increased receptor levels. In addition, α myosin heavy chain levels decreased and β myosin heavy chain levels increased in all 3 of the senescent groups. In rodents, α myosin heavy chain is the predominant isoform, and a shift in isoforms is a marker of cardiac hypertrophy.2 Estrogen attenuated the decrease in α myosin heavy chain in young ovariectomized rats but not senescent rats. Together, these data implicate an age-related loss in cardiac estrogen sensitivity with the development of cardiac hypertrophy. That the same levels of estrogen can have differential effects on …
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