Hypertension Research Today is a free monthly online journal that collates and summarizes the latest research about Hypertension, including details on symptoms, diagnosis, diet, treatment, causes. | ||||||||
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Role of endothelin in mediating postmenopausal hypertension in a rat model.Yanes LL, Romero DG, Cucchiarelli VE, Fortepiani LA, Gomez-Sanchez CE, Santacruz F, Reckelhoff JF Department of Physiology and Biophysics, University of Mississippi Medical Center, 2500 N. State St., Jackson, MS 39216-4505, USA. 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(A)R) 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(A)R antagonist ABT-627 (5 mg.kg(-1).day(-1)). BP was significantly higher in PMR than in YF. ET(A)R antagonist reduced BP in PMR by 20% to the level found in control YF. ET(A)R 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(A)R. Published 13 December 2004 in Am J Physiol Regul Integr Comp Physiol, 288(1): R229-33.
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