Role of endothelin in mediating postmenopausal hypertension in a rat model

Licy L. Yanes, Damian G. Romero, Valeria E. Cucchiarelli, Lourdes A. Fortepiani, Celso E. Gomez-Sanchez, Francisco Santacruz, Jane F. Reckelhoff

Research output: Contribution to journalArticlepeer-review

51 Scopus citations


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 ETA receptor (ETAR) 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 ETAR antagonist ABT-627 (5 mg·kg-1·day -1). BP was significantly higher in PMR than in YF. ETAR 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 ETAR.

Original languageEnglish (US)
Pages (from-to)R229-R233
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Issue number1 57-1
StatePublished - Jan 2005
Externally publishedYes


  • ET receptor
  • ET receptor
  • Kidney

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)


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