{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T18:16:52Z","timestamp":1789755412318,"version":"4.0.1"},"reference-count":33,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2001,4,1]]},"abstract":"<jats:p>\n                    Uterine blood flow (UBF) and uterine artery endothelial nitric oxide synthase (eNOS) expression are greatest during the follicular vs. luteal phase. 17\u03b2-Estradiol (E\n                    <jats:sub>2<\/jats:sub>\n                    \u03b2) increases UBF and elevates eNOS in ovine uterine but not systemic arteries; progesterone (P\n                    <jats:sub>4<\/jats:sub>\n                    ) effects on E\n                    <jats:sub>2<\/jats:sub>\n                    \u03b2 changes of eNOS remain unclear. Nonpregnant ovariectomized sheep received either vehicle ( n = 10), P\n                    <jats:sub>4<\/jats:sub>\n                    (0.9 g Controlled Internal Drug Release vaginal implants; n = 13), E\n                    <jats:sub>2<\/jats:sub>\n                    \u03b2 (5 \u03bcg\/kg bolus + 6 \u03bcg \u00b7 kg\n                    <jats:sup>\u22121<\/jats:sup>\n                    \u00b7 day\n                    <jats:sup>\u22121<\/jats:sup>\n                    ; n = 10), or P\n                    <jats:sub>4<\/jats:sub>\n                    + E\n                    <jats:sub>2<\/jats:sub>\n                    \u03b2 ( n = 12). Reproductive (uterine\/mammary) and nonreproductive (omental\/renal) artery endothelial proteins were procured on day 10, and eNOS was measured by Western analysis. P\n                    <jats:sub>4<\/jats:sub>\n                    and E\n                    <jats:sub>2<\/jats:sub>\n                    \u03b2 alone and in combination increased ( P &lt; 0.05) eNOS expression in uterine artery endothelium (vehicle = 100 \u00b1 16%, P\n                    <jats:sub>4<\/jats:sub>\n                    = 251 \u00b1 59%, E\n                    <jats:sub>2<\/jats:sub>\n                    \u03b2 = 566 \u00b1 147%, P\n                    <jats:sub>4<\/jats:sub>\n                    + E\n                    <jats:sub>2<\/jats:sub>\n                    \u03b2 = 772 \u00b1 211% of vehicle). Neither omental, renal, nor mammary artery eNOS was altered, demonstrating the local nature of steroid-induced maintenance of uterine arterial eNOS. In the myometrial microvasculature, eNOS was increased slightly ( P = 0.06) with E\n                    <jats:sub>2<\/jats:sub>\n                    \u03b2 and significantly with P\n                    <jats:sub>4<\/jats:sub>\n                    + E\n                    <jats:sub>2<\/jats:sub>\n                    \u03b2. Systemic NO\n                    <jats:sub>x<\/jats:sub>\n                    was increased with P\n                    <jats:sub>4<\/jats:sub>\n                    and P\n                    <jats:sub>4<\/jats:sub>\n                    + E\n                    <jats:sub>2<\/jats:sub>\n                    \u03b2, but not E\n                    <jats:sub>2<\/jats:sub>\n                    \u03b2, suggesting differential regulation of eNOS expression and activity, since P\n                    <jats:sub>4<\/jats:sub>\n                    increased eNOS in uterine artery endothelium while E\n                    <jats:sub>2<\/jats:sub>\n                    \u03b2 and the combination further increased eNOS protein.\n                  <\/jats:p>","DOI":"10.1152\/ajpheart.2001.280.4.h1699","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T13:14:34Z","timestamp":1513948474000},"page":"H1699-H1705","source":"Crossref","is-referenced-by-count":88,"title":["Endothelial vasodilator production by uterine and systemic arteries. VII. Estrogen and progesterone effects on eNOS"],"prefix":"10.1152","volume":"280","author":[{"given":"Heidi L.","family":"Rupnow","sequence":"first","affiliation":[{"name":"Departments of Obstetrics and Gynecology, Perinatal Research Laboratories, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Terrance M.","family":"Phernetton","sequence":"additional","affiliation":[{"name":"Departments of Obstetrics and Gynecology, Perinatal Research Laboratories, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cynthia E.","family":"Shaw","sequence":"additional","affiliation":[{"name":"Departments of Obstetrics and Gynecology, Perinatal Research Laboratories, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mary L.","family":"Modrick","sequence":"additional","affiliation":[{"name":"Departments of Obstetrics and Gynecology, Perinatal Research Laboratories, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ian 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