Role of angiotensin II and α-adrenergic receptors during estrogen-induced vasodilation in ewes

L. E. Davis, R. R. Magness, C. R. Rosenfeld

Research output: Contribution to journalArticle

14 Scopus citations

Abstract

Estradiol-17β (E2β) produces uterine and systemic vasodilation in nonpregnant ewes without altering mean arterial pressure (MAP). Mechanisms responsible for maintaining MAP and thus uterine blood flow (UBF) may include activation of the renin-angiotensin and/or adrenergic systems. We therefore investigated the effects of systemic blockade of angiotensin II (ANG II) and/or α-adrenergic receptors in nonpregnant, castrated ewes, using saralasin (Sar) and/or phentolamine (Phen) in the presence or absence of intravenous E2β (1.0 μg/kg). In nonestrogenized ewes neither antagonist alone had substantial cardiovascular effects; however, Sar + Phen decreased systemic vascular resistance (SVR) 20 ± 7.4% (SE) and increased heart rate (HR) 50 ± 19% (P < 0.01); MAP and UBF were unaffected. Following E2β treatment SVR fell 17 ± 2.4% (P < 0.01), UBF increased more than fourfold, and MAP was unchanged. Compared with E2β alone, Phen + E2β decreased SVR 42 ± 4.7%, and MAP fell 11 ± 1.8% (P < 0.05) despite 40-50% increases in HR and cardiac output (P < 0.05). Responses to Sar + E2β were similar to E2β alone, except for a fall in MAP, whereas responses to Sar + Phen + E2β resembled those of Phen + E2β. E2β-induced uterine vasodilation was unaltered by Sar and/or Phen. During E2β-induced vasodilation, MAP is maintained by enhanced activation of the α-adrenergic and renin-angiotensin systems; however, uterine vascular responses to E2β are independent of both systems and perfusion pressure.

Original languageEnglish (US)
Pages (from-to)E837-E843
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Volume263
Issue number5 26-5
StatePublished - Jan 1 1992

Keywords

  • blood pressure control
  • cardiac output
  • heart rate
  • uterine blood flow

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Physiology
  • Physiology (medical)

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