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Basic Science Investigations |
1 Division of Nuclear Medicine, Johns Hopkins University, Baltimore, Maryland
2 Division of Nephrology and Hypertension, Georgetown University, Washington, DC
3 Division of Comparative Medicine, Johns Hopkins University, Baltimore, Maryland
The renin angiotensin system (RAS) has been implicated as one mediator of the cardiovascular effects of estrogen. Since changes in angiotensin type 1 (AT1) receptor expression are central to modulation of the RAS, we used the noninvasive PET imaging technique to study for the in vivo effects of estrogen on membrane and intracellular AT1 receptors. Methods: Dynamic PET measurements of canine AT1 (cAT1) receptors using the radiolabeled AT1 receptor antagonist, 11C-L-159,884, were performed during 2-wk consecutive periods of estrogen deprivation induced by ovariectomy and 17ß-estradiol (E2) replacement. Results: Kinetic modeling of time-activity curves in the kidney and adrenal showed lower receptor expression in the estrogen replete state (21% and 30% decrease in Gjedde-Patlak slope, influx constant, respectively). These in vivo findings correlated with in vitro radioligand-binding assays with 125I-[Sar1,Ile8]angiotensin II showing reduced AT1 receptor number in the adrenal (35%), glomeruli (30%), myocardium (35%), and liver (21%) in the estrogen-replenished compared with estrogen-depleted animals. Conclusion: Although other endogenous systems are known to regulate AT1 receptors and could compete with estrogenic actions, these PET studies reveal that estrogen attenuates AT1 receptor expression in vivo. Thus, estrogen modulation of AT1 receptors may contribute to the cardiovascular protective effects associated with estrogen.
Key Words: estrogen • renin angiotensin system • PET • AT1 receptor • angiotensin receptor • estrogen • hormone replacement therapy • adrenal • kidney • heart • liver • regulation • expression
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