Endothelium-derived nitric oxide synthase protein expression in ovine placental arteries

Citation
C. Sheppard et al., Endothelium-derived nitric oxide synthase protein expression in ovine placental arteries, BIOL REPROD, 64(5), 2001, pp. 1494-1499
Citations number
27
Categorie Soggetti
da verificare
Journal title
BIOLOGY OF REPRODUCTION
ISSN journal
00063363 → ACNP
Volume
64
Issue
5
Year of publication
2001
Pages
1494 - 1499
Database
ISI
SICI code
0006-3363(200105)64:5<1494:ENOSPE>2.0.ZU;2-M
Abstract
During the third trimester, fetoplacental and uterine blood flows increase dramatically to meet the high metabolic demands of the growing fetus. We hy pothesized that the expression of endothelial nitric oxide synthase (eNOS) in fetoplacental artery endothelium and the concentrations of nitric oxide (NO) and cyclic CMP (cGMP) in amniotic fluid (AF) are increased during the third trimester of ovine gestation. Placental arteries and AF were collecte d from ewes at 110, 120, 130, and 142 days of gestation (n = 24; mean +/- S EM term = 145 +/- 3 days). Expression of eNOS protein was measured in intac t and denuded placental arteries and in endothelium-derived protein by West ern analysis and confirmed by immunohistochemistry. Concentrations of NO (n itrates plus nitrites) and cGMP were determined in AF. Placental artery eNO S protein expression was localized to the endothelium, where it was markedl y greater than in vascular smooth muscle. Placental artery endothelium-deri ved eNOS expression and AF cGMP concentrations were similar at 110 and 120 days of gestation; however, both peaked at 130 days at levels two- to three fold above baseline (P < 0.05) before returning to baseline at 142 days of pregnancy. The AF NO (nitrates plus nitrites) levels, however, increased pr ogressively between 120 days of gestation and term (P < 0.05). We concluded that endothelium-derived placental artery eNOS levels, AF NO (nitrates plu s nitrites), and AF cGMP were markedly increased during the third trimester , thus supporting a role for NO-mediated elevations in cGMP in the control of fetoplacental blood flow.