{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,11]],"date-time":"2025-10-11T17:49:06Z","timestamp":1760204946867,"version":"3.37.3"},"reference-count":58,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2018,2,16]],"date-time":"2018-02-16T00:00:00Z","timestamp":1518739200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["AA19446","AA23520","AA23035"],"award-info":[{"award-number":["AA19446","AA23520","AA23035"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Alcoholism Clin &amp;amp; Exp Res"],"published-print":{"date-parts":[[2018,4]]},"abstract":"<jats:sec><jats:title>Background<\/jats:title><jats:p>A cardinal feature of fetal alcohol syndrome is growth restriction. Maternal uterine artery adaptations to pregnancy correlate with birthweight and survival. We hypothesized that gestational binge alcohol exposure impairs maternal uterine vascular function, affecting endothelial nitric oxide (NO)\u2010mediated vasodilation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Pregnant rats grouped as pair\u2010fed control or binge alcohol exposed received a once\u2010daily, orogastric gavage of isocaloric maltose\u2013dextrin or alcohol, respectively. On gestational day 20, primary uterine arteries were isolated, cannulated, and connected to a pressure transducer, and functional studies were conducted by dual\u2010chamber arteriography. Uterine arteries maintained at constant intramural pressure (90\u00a0mm Hg) were maximally constricted with thromboxane, and a dose\u2013response for acetylcholine (Ach) was recorded.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The alcohol group exhibited significantly impaired endothelium\u2010dependent, Ach\u2010induced uterine artery relaxation (\u2193\u223c30%). Subsequently, a dose\u2013response was recorded following inhibition of endothelium\u2010derived hyperpolarizing factor (apamin and TRAM\u201034) and prostacyclin (indomethacin). Ach\u2010induced relaxation in the pair\u2010fed control decreased by ~46%, and interestingly, relaxation in alcohol group further decreased by an additional ~48%, demonstrating that gestational binge alcohol impairs the NO system in the primary uterine artery. An endothelium\u2010independent sodium nitroprusside effect was not observed. Immunoblotting indicated that alcohol decreased the level of endothelial excitatory P\u2010Ser<jats:sup>1177<\/jats:sup> endothelial NO synthase (eNOS) (<jats:italic>p\u00a0<\/jats:italic>&lt;<jats:italic>\u00a0<\/jats:italic>0.05) and total eNOS expression (<jats:italic>p\u00a0<\/jats:italic>&lt;<jats:italic>\u00a0<\/jats:italic>0.05) compared to both the normal and pair\u2010fed controls. P\u2010Ser<jats:sup>1177<\/jats:sup>eNOS level was also confirmed by immunofluorescence imaging.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>This is the first study to demonstrate maternal binge alcohol consumption during pregnancy disrupts uterine artery vascular function via impairment of the eNOS vasodilatory system.<\/jats:p><\/jats:sec>","DOI":"10.1111\/acer.13602","type":"journal-article","created":{"date-parts":[[2018,1,24]],"date-time":"2018-01-24T13:13:14Z","timestamp":1516799594000},"page":"682-690","source":"Crossref","is-referenced-by-count":12,"title":["Mechanisms Underlying Chronic Binge Alcohol Exposure\u2010Induced Uterine Artery Dysfunction in Pregnant Rat"],"prefix":"10.1111","volume":"42","author":[{"given":"Vishal D.","family":"Naik","sequence":"first","affiliation":[{"name":"Department of Veterinary Physiology and Pharmacology College of Veterinary Medicine and Biomedical Sciences Texas A&amp;M University College Station 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