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Am J Physiol Heart Circ Physiol 248: H339-H344, 1985;
0363-6135/85 $5.00
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AJP - Heart and Circulatory Physiology, Vol 248, Issue 3 339-H344, Copyright © 1985 by American Physiological Society

ARTICLES

Role of alpha-receptors in estrogen-induced vasodilation in nonpregnant sheep

R. P. Naden and C. R. Rosenfeld

Estradiol-17 beta (E2) produces vasodilation in several systemic vascular beds, but most extensively in the nonpregnant uterus. It has been postulated that E2 induces this vasodilation via blockade of vascular alpha-adrenergic receptors. This hypothesis was tested in six chronically instrumented, nonpregnant sheep by comparing the systemic and uterine hemodynamic responses to intravenous E2, to an alpha-adrenergic receptor blocker, phentolamine, and to both agents given together. Uterine blood flow (UBF) increased significantly after E2 administration, from 20 +/- 7 to 233 +/- 37 (SE) ml/min. In contrast, phentolamine had no detectable effect on UBF or on the UBF response to E2 when both were given together. Similar contrasting responses were observed in the effects of E2 and/or phentolamine on the systemic vasculature. When responses to alpha-agonists were evaluated, there was no evidence of alpha-blockade following E2 despite the substantial vasodilation; in contrast, alpha-blockade was present during phentolamine administration when no vasodilation was noted. Therefore, we conclude that E2-induced vasodilation in chronically instrumented sheep is not mediated through blockade of vascular alpha-adrenergic receptors.


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B. E. Cox, T. A. Roy, and C. R. Rosenfeld
Angiotensin II mediates uterine vasoconstriction through {alpha}-stimulation
Am J Physiol Heart Circ Physiol, July 1, 2004; 287(1): H126 - H134.
[Abstract] [Full Text] [PDF]


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