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(Hypertension. 2007;50:768.)
© 2007 American Heart Association, Inc.
XVIIth Scientific Meeting of the Inter-American Society of Hypertension |
and Estrogen Receptor-ß in Young Salt-Sensitive and -Resistant RatsFrom the Department of Anesthesiology, University of Texas Health Science Center at San Antonio.
Correspondence to Carmen Hinojosa-Laborde, PhD, Department of Anesthesiology, University of Texas Health Science Center, 7703 Floyd Curl Dr, San Antonio, TX 78229-3900. E-mail laborde{at}uthscsa.edu
This study evaluated the effect of ovariectomy on renal estrogen receptor (ER)-
and ERß expression in young female Dahl salt-sensitive and salt-resistant rats. Our hypothesis was that estrogen depletion results in an imbalance in ER
and ERß expression in salt-sensitive rats. Rats were subjected to sham surgery (intact), ovariectomy, and ovariectomy with estrogen replacement. Kidneys were harvested 8 weeks later. Western blot was used to measure ER
and ERß expression in the cortex and medulla. In intact rats, ER
was 2.7- and 4.3-fold higher in salt-sensitive compared with salt-resistant rats in the renal cortex and medulla, respectively. In salt-sensitive rats, ovariectomy caused 42% and 52% decreases in ER
and 107% and 314% increases in ERß in renal cortex and medulla, respectively. In salt-resistant rats, ovariectomy caused 33% and 150% increases in ER
and 107% and 100% increases in ERß in renal cortex and medulla, respectively. Estrogen replacement did not alter ER
but restored ERß expression levels similar to levels in intact rats in both salt-sensitive and salt-resistant rats. Thus, estrogen loss had opposite effects on ER
in salt-sensitive (downregulation) and salt-resistant rats (upregulation). We propose that the decrease in ER
expression in salt-sensitive rats after estrogen loss alters the balance of renal ERs and may play a role in accelerating the development of hypertension and renal damage.
Key Words: Dahl rats salt sensitivity hypertension estrogens estrogen receptors kidney
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