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attractive. However, only equivocal support for such a mechanism presently exists. For example, decreased tisH344,1985.-Estradiol-17p (E2) producesvasodilation in sev- sue concentrations of a-receptors have been reported in eral systemicvascular beds,but most extensively in the non- the presence of estrogen (8,X), but in several studies an pregnant uterus. It has been postulated that E2 induces this increase in a-receptors has been noted (14, 15, 20). vasodilation via blockade of vascular cu-adrenergic receptors. Furthermore, estrogen treatment has been shown both This hypothesis was tested in six chronically instrumented, nonpregnant sheep by comparing the systemic and uterine to increase (3) and decrease (10) tissue levels of cateresults have also come from in hemodynamicresponses intravenous E2, to an cu-adrenergic cholamines. Conflicting to receptor blocker, phentolamine, and to both agents given to- vivo studies in which compounds that block a-adrenergic gether. Uterine blood flow (UBF) increasedsignificantly after receptors were used. Although in some studies (5, 6) E2 administration, from 20 & 7 to 233 t 37 (SE) ml/min. In treatment with a-blocking agents was followed by uterine contrast, phentolamine had no detectable effect on UBF or on vasodilation similar to that produced by estrogen, this the UBF response E2 when both were given
AJP - Heart and Circulatory Physiology – The American Physiological Society
Published: Mar 1, 1985
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