Endothelial vasodilator production by uterine and systemic arteries. III. Ovarian and estrogen effects on NO synthase

• Published in: American journal of physiology. Heart and circulatory physiology 1998-11, Vol.275 (5), p.H1845-H1856
• Main Authors: Vagnoni, Karen E, Shaw, Cynthia E, Phernetton, Terrance M, Meglin, Beth M, Bird, Ian M, Magness, Ronald R
• Format: Article
• Language: English
• ISSN: 0363-6135; 1522-1539
• DOI: 10.1152/ajpheart.1998.275.5.H1845

1  Perinatal Research Laboratories, Department of Obstetrics and Gynecology, and 2  Department of Meat and Animal Science, University of Wisconsin-Madison Medical School, Madison, Wisconsin 53715 During the follicular phase of the ovarian cycle, when the local estrogen-to-progesterone ratio is elevated, uterine blood flow is elevated. This vasodilatory response is reproduced by exogenous 17 -estradiol (E 2 ) administration via a nitric oxide (NO)-mediated mechanism. We hypothesized that endogenous ovarian estrogen and exogenous E 2 treatment elevate expression of endothelial cell-derived NO synthase (eNOS) in uterine, but not in systemic, arteries. Uterine, mammary, and systemic (renal and/or omental) arteries were collected from 1 ) ewes synchronized to the follicular ( day 1 to day 0 ) or luteal ( day 10 ) phases of the ovarian cycle ( n  = 4 per phase), 2 ) ovariectomized ewes 120 min after systemic vehicle or E 2 (5 µg/kg iv) treatment, and 3 ) ovariectomized ewes on days 0 , 3 , 6 , 8 , and 10  of E 2 (5 µg/kg iv, followed by 6 µg/kg per day) treatment. Expression of eNOS was localized primarily to the endothelium rather than vascular smooth muscle (VSM) in all arteries examined by immunohistochemistry and Western analysis; inducible NOS was not detected in either endothelium or VSM. Expression of eNOS protein was greater ( P