Local and systemic estradiol-17β

Effects on uterine and systemic vasodilation

R. R. Magness, C. R. Rosenfeld

Research output: Contribution to journalArticle

246 Citations (Scopus)

Abstract

Systemic estradiol-17β (E2β) administration increases uterine blood flow (UBF), cardiac output (CO), heart rate (HR), and plasma renin activity (PRA). We sought to determine if the E2β-induced systemic responses were dependent on the observed uterine responses. Nonpregnant, ovariectomized ewes (n = 5) received 3 μg E2β into both uterine arteries followed 120 min later by systemic E2β, 1 μg/kg. At 120 min after local E2β, UBF increased from 26 ± 5 to 161 ± 21 ml/min (P < 0.05); uterine vascular resistance (UVR) decreased 83 ± 2.5% (P < 0.05); and systemic parameters were unchanged. At 120 min after systemic E2β, UBF remained elevated and CO had increased gradually from 4.4 ± 0.2 to 5.5 ± 0.32 l/min (26 ± 3.4%, P < 0.05), reflecting a 37 ± 3.9% (P < 0.05) increase in HR, mean arterial pressure (MAP) remained unchanged. The increased CO was associated with a 20 ± 3.1% (P < 0.05) fall in systemic vascular resistance (SVR), with %ΔSVR < %ΔUVR (P < 0.05). Base-line PRA and angiotensin II, 1.31 ± 0.2 ng · ml-1 · h-1 and 10.3 ± 2.1 pg/ml, respectively, were unchanged by local E2β; systemic E2β caused increases to 3.56 ± 0.51 ng · ml-1 · h-1 (P < 0.05) and 34.1 ± 11.3 pg/ml (P < 0.05), respectively. E2β-induced uterine hyperemia occurs independent of its systemic effects and is not responsible for systemic cardiovascular alterations, and the relative uterine vascular responses exceed systemic responses. Systemic responses, e.g., heart rate-mediated increases in CO, are associated with maintenance of MAP, decreases in SVR, and increases in PRA and angiotensin II that are not of uterine origin.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Volume256
Issue number4
StatePublished - 1989

Fingerprint

Renin
Vasodilation
Vascular Resistance
Estradiol
Blood
Cardiac Output
Plasmas
Angiotensin II
Heart Rate
Arterial Pressure
Uterine Artery
Hyperemia
Blood Vessels
Maintenance

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology
  • Physiology

Cite this

@article{b8878c154e49408eb28ed54c9a6ba7f5,
title = "Local and systemic estradiol-17β: Effects on uterine and systemic vasodilation",
abstract = "Systemic estradiol-17β (E2β) administration increases uterine blood flow (UBF), cardiac output (CO), heart rate (HR), and plasma renin activity (PRA). We sought to determine if the E2β-induced systemic responses were dependent on the observed uterine responses. Nonpregnant, ovariectomized ewes (n = 5) received 3 μg E2β into both uterine arteries followed 120 min later by systemic E2β, 1 μg/kg. At 120 min after local E2β, UBF increased from 26 ± 5 to 161 ± 21 ml/min (P < 0.05); uterine vascular resistance (UVR) decreased 83 ± 2.5{\%} (P < 0.05); and systemic parameters were unchanged. At 120 min after systemic E2β, UBF remained elevated and CO had increased gradually from 4.4 ± 0.2 to 5.5 ± 0.32 l/min (26 ± 3.4{\%}, P < 0.05), reflecting a 37 ± 3.9{\%} (P < 0.05) increase in HR, mean arterial pressure (MAP) remained unchanged. The increased CO was associated with a 20 ± 3.1{\%} (P < 0.05) fall in systemic vascular resistance (SVR), with {\%}ΔSVR < {\%}ΔUVR (P < 0.05). Base-line PRA and angiotensin II, 1.31 ± 0.2 ng · ml-1 · h-1 and 10.3 ± 2.1 pg/ml, respectively, were unchanged by local E2β; systemic E2β caused increases to 3.56 ± 0.51 ng · ml-1 · h-1 (P < 0.05) and 34.1 ± 11.3 pg/ml (P < 0.05), respectively. E2β-induced uterine hyperemia occurs independent of its systemic effects and is not responsible for systemic cardiovascular alterations, and the relative uterine vascular responses exceed systemic responses. Systemic responses, e.g., heart rate-mediated increases in CO, are associated with maintenance of MAP, decreases in SVR, and increases in PRA and angiotensin II that are not of uterine origin.",
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T2 - Effects on uterine and systemic vasodilation

AU - Magness, R. R.

AU - Rosenfeld, C. R.

PY - 1989

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N2 - Systemic estradiol-17β (E2β) administration increases uterine blood flow (UBF), cardiac output (CO), heart rate (HR), and plasma renin activity (PRA). We sought to determine if the E2β-induced systemic responses were dependent on the observed uterine responses. Nonpregnant, ovariectomized ewes (n = 5) received 3 μg E2β into both uterine arteries followed 120 min later by systemic E2β, 1 μg/kg. At 120 min after local E2β, UBF increased from 26 ± 5 to 161 ± 21 ml/min (P < 0.05); uterine vascular resistance (UVR) decreased 83 ± 2.5% (P < 0.05); and systemic parameters were unchanged. At 120 min after systemic E2β, UBF remained elevated and CO had increased gradually from 4.4 ± 0.2 to 5.5 ± 0.32 l/min (26 ± 3.4%, P < 0.05), reflecting a 37 ± 3.9% (P < 0.05) increase in HR, mean arterial pressure (MAP) remained unchanged. The increased CO was associated with a 20 ± 3.1% (P < 0.05) fall in systemic vascular resistance (SVR), with %ΔSVR < %ΔUVR (P < 0.05). Base-line PRA and angiotensin II, 1.31 ± 0.2 ng · ml-1 · h-1 and 10.3 ± 2.1 pg/ml, respectively, were unchanged by local E2β; systemic E2β caused increases to 3.56 ± 0.51 ng · ml-1 · h-1 (P < 0.05) and 34.1 ± 11.3 pg/ml (P < 0.05), respectively. E2β-induced uterine hyperemia occurs independent of its systemic effects and is not responsible for systemic cardiovascular alterations, and the relative uterine vascular responses exceed systemic responses. Systemic responses, e.g., heart rate-mediated increases in CO, are associated with maintenance of MAP, decreases in SVR, and increases in PRA and angiotensin II that are not of uterine origin.

AB - Systemic estradiol-17β (E2β) administration increases uterine blood flow (UBF), cardiac output (CO), heart rate (HR), and plasma renin activity (PRA). We sought to determine if the E2β-induced systemic responses were dependent on the observed uterine responses. Nonpregnant, ovariectomized ewes (n = 5) received 3 μg E2β into both uterine arteries followed 120 min later by systemic E2β, 1 μg/kg. At 120 min after local E2β, UBF increased from 26 ± 5 to 161 ± 21 ml/min (P < 0.05); uterine vascular resistance (UVR) decreased 83 ± 2.5% (P < 0.05); and systemic parameters were unchanged. At 120 min after systemic E2β, UBF remained elevated and CO had increased gradually from 4.4 ± 0.2 to 5.5 ± 0.32 l/min (26 ± 3.4%, P < 0.05), reflecting a 37 ± 3.9% (P < 0.05) increase in HR, mean arterial pressure (MAP) remained unchanged. The increased CO was associated with a 20 ± 3.1% (P < 0.05) fall in systemic vascular resistance (SVR), with %ΔSVR < %ΔUVR (P < 0.05). Base-line PRA and angiotensin II, 1.31 ± 0.2 ng · ml-1 · h-1 and 10.3 ± 2.1 pg/ml, respectively, were unchanged by local E2β; systemic E2β caused increases to 3.56 ± 0.51 ng · ml-1 · h-1 (P < 0.05) and 34.1 ± 11.3 pg/ml (P < 0.05), respectively. E2β-induced uterine hyperemia occurs independent of its systemic effects and is not responsible for systemic cardiovascular alterations, and the relative uterine vascular responses exceed systemic responses. Systemic responses, e.g., heart rate-mediated increases in CO, are associated with maintenance of MAP, decreases in SVR, and increases in PRA and angiotensin II that are not of uterine origin.

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M3 - Article

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JO - American Journal of Physiology - Heart and Circulatory Physiology

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