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NEUROHUMORAL CONTROL OF CARDIOVASCULAR FUNCTION

Role of endothelin in mediating postmenopausal hypertension in a rat model

Departments of ¹Physiology and Biophysics and ²Medicine, University of Mississippi Medical Center, Jackson, Mississippi; and ³Department of Medicine and Pathophysiology, National Hospital of Paraguay, Asunción, Paraguay

Submitted 5 December 2003 ; accepted in final form 17 August 2004

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, postestrous-cycling (PMR) spontaneously hypertensive rats (SHR) as a model of postmenopausal hypertension. The purpose of the present study was to determine whether endothelin plays a role in the increased BP in PMR. Premenopausal female SHR, aged 4–5 mo (YF), and PMR, aged 16 mo, 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 in renal cortex of YF, but there was no difference in medullary ET-1. Expression of endothelin ET_A receptor (ET_AR) mRNA was lower in renal cortex and medulla of PMR than of YF. Additional groups of rats (n = 6–7/group) were treated for 3 wk with the ET_AR antagonist ABT-627 (5 mg·kg^–1·day^–1). BP was significantly higher in PMR than in YF. ET_AR antagonist reduced BP in PMR by 20% to the level found in control YF. ET_AR 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 ET_AR.

ET_A receptor; ET_B receptor; kidney

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