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AJP - Endocrinology and Metabolism, Vol 256, Issue 4 E536-E542, Copyright © 1989 by American Physiological Society
ARTICLES |
R. R. Magness and C. R. Rosenfeld
Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas 75235.
Systemic estradiol-17 beta (E2 beta) administration increases uterine blood flow (UBF), cardiac output (CO), heart rate (HR), and plasma renin activity (PRA). We sought to determine if the E2 beta-induced systemic responses were dependent on the observed uterine responses. Nonpregnant, ovariectomized ewes (n = 5) received 3 micrograms E2 beta into both uterine arteries followed 120 min later by systemic E2 beta, 1 microgram/kg. At 120 min after local E2 beta, UBF increased from 26 +/- 5 to 161 +/- 21 ml/min (P less than 0.05); uterine vascular resistance (UVR) decreased 83 +/- 2.5% (P less than 0.05); and systemic parameters were unchanged. At 120 min after systemic E2 beta, UBF remained elevated and CO had increased gradually from 4.4 +/- 0.2 to 5.5 +/- 0.32 l/min (26 +/- 3.4%, P less than 0.05), reflecting a 37 +/- 3.9% (P less than 0.05) increase in HR; mean arterial pressure (MAP) remained unchanged. The increased CO was associated with a 20 +/- 3.1% (P less than 0.05) fall in systemic vascular resistance (SVR), with % delta SVR less than % delta UVR (P less than 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 E2 beta; systemic E2 beta caused increases to 3.56 +/- 0.51 ng.ml-1.h-1 (P less than 0.05) and 34.1 +/- 11.3 pg/ml (P less than 0.05), respectively. E2 beta-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.(ABSTRACT TRUNCATED AT 250 WORDS)
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