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1 Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS, USA
2 Medicine, University of Mississippi Medical Center, Jackson, MS, USA
3 Medicine and Pathophysiology, National Hospital of Paraguay, Asuncion, Paraguay
* To whom correspondence should be addressed. E-mail: jreckelhoff{at}physiology.umsmed.edu.
Cardiovascular disease is the leading cause of death in women after menopause. Hypertension, a major cardiovascular risk factor, becomes more prevalent after menopause. The mechanisms responsible for the increase in blood pressure (BP) in postmenopausal women are unknown. We have recently characterized the aged, post-estrous-cycling SHR (PMR) as a model of post-menopausal hypertension. The purpose of the present study was to determine if endothelin plays a role in the increased BP in PMR. Premenopausal female SHR, aged 4-5 mos (YF) and postmenopausal SHR (PMR), aged 16 mos, were studied. Expression of preproendothelin-1 mRNA was not different in either renal cortex or medulla between PMR and YF (n=7-8/group). In contrast ET-1 peptide expression was significantly higher in renal cortex of PMR than YF, but there was no difference in medullary ET-1. Expression of endothelin ETA receptor (ETAR) mRNA was lower in renal cortex and medulla of PMR than YF. Additional groups of rats (n=6-7/group) were treated for 3 wks with the ETAR antagonist, ABT 627 (5 mg/kg/d). BP was significantly higher in PMR than YF. ETAR antagonist reduced BP in PMR by 20% to the level found in control YF. ETAR antagonist had no effect on BP in YF. These data support the hypothesis that the increase in BP in PMR is mediated in part by endothelin and the ETAR.
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