Systemic estradiol-17 beta (E2 beta) administration increases uterine blood flow (UBF), cardiac output (CO), heart rate (HR), and plasma renin activity (PRA). We sought to determine if the E2 beta-induced systemic responses were dependent on observed responses. Nonpregnant, ovariectomized ewes (n = 5) received 3 micrograms into both arteries followed 120 min later by beta, 1 microgram/kg. At after local UBF increased from 26 +/- 5 161 21 ml/min (P less than 0.05); vascular resistance (UVR)...

Estradiol-17beta (E2beta), a potent vasodilator, has its greatest effects on the uterine vasculature, blood flow (UBF) increasing > or = 10-fold. The mechanism(s) responsible for E2beta-induced vasodilation is unclear. We determined if nitric oxide (NO)-induced increases in cGMP modulate estrogen-induced UBF, and cyclooxygenase inhibition modifies E2beta responses. Nonpregnant (n 15) pregnant 8) ewes had probes implanted main arteries catheters branches of vein artery bilaterally sampling...

Estrogens and estrogen metabolites have important functions in cardiovascular other physiology, yet the patterns of synthesis, metabolism, individual plasma profile estrogens during human pregnancy as well preeclampsia remain undetermined. We performed liquid chromatography mass spectrometry on samples from normotensive pregnant women (normP; n=8), with mild (mPE; severe (sPE; n = 8) at labor. Compared normP, estrone was lower sPE, whereas level estradiol-17β significantly mPE sPE. Estriol...

Studies in rats and mice have established that maternal nutrition induces epigenetic modifications, sometimes permanently, alter gene expression the fetus, which turn leads to phenotypic changes. However, limited data is available on influence of diet modifications sheep. Therefore, objectives this study were investigate impact different dietary energy sources imprinted genes fetuses Ewes naturally bred a single sire from days 67 ± 3 gestation until necropsy (days 130 1), they fed one three...

Rapid uterine vasodilatation after estrogen administration is believed to be mediated by endothelial production of nitric oxide (NO) via NO synthase (eNOS). However, the mechanism(s) which activates eNOS in artery cells (UAEC) unknown. In this study, we observed that estradiol-17beta (E2) and E2-BSA rapidly (<2 min) increased total NOx UAEC vitro. This was associated with rapid phosphorylation activation but unaltered pretreatment actinomycin-D. Estrogen receptor-alpha protein detectable...

Vascular endothelial growth factor (VEGF) is a potent regulator of placental vascular function. Endothelial dysfunction key associated with preeclampsia. In this study, we examined expression VEGF, endocrine gland-derived VEGF (EG-VEGF), receptors 1 and 2 (VEGFR-1 VEGFR-2), neuropilin-1 -2 (NP-1 NP-2) in human placentas from women normal preeclamptic (PE) pregnancies using quantitative or semiquantitative PCR. We found that total mRNA was increased 2.8-fold (P < 0.05), along increases...

Angiotensin II has been identified immunohistochemically in the ovaries of both rats and humans. Here we present evidence that angiotensin (an extremely vasoactive agent a wide range tissues) may be involved regulation major steroidogenic enzyme ovary, cholesterol side chain cleavage cytochrome P-450 (P-450scc), as well basic fibroblast growth factor (bFGF), which implicated an angiogenic bovine corpus luteum. We have used primary cultures luteal cells to examine effect its receptor...

Preeclampsia (PE) is a common cause of maternal morbidity, characterized by impaired trophoblast invasion and spiral artery transformation resulting in progressive uteroplacental hypoxia. Given the primary role LIN28A LIN28B modulating cell metabolism, differentiation, invasion, we hypothesized that and/or regulates differentiation its dysregulation may contribute to PE. Here show expressed ∼1300-fold higher than human term placenta predominant paralog cultures. The expression mRNA protein...

Uterine blood flow (UBF) and uterine artery endothelial nitric oxide synthase (eNOS) expression are greatest during the follicular vs. luteal phase. 17β-Estradiol (E 2 β) increases UBF elevates eNOS in ovine but not systemic arteries; progesterone (P 4 ) effects on E β changes of remain unclear. Nonpregnant ovariectomized sheep received either vehicle ( n = 10), P (0.9 g Controlled Internal Drug Release vaginal implants; 13), (5 μg/kg bolus + 6 μg · kg −1 day ; or 12). Reproductive...

During pregnancy, the uterine vasculature shows a marked increase in vasodilator production [prostacyclin (PGI2) and nitric oxide (NO)] response to number of agonists including angiotensin II (AII) ATP. As consequence vascular resistance is kept low, blood flow maximized meet needs growing fetus. Studies molecular basis underlying this change control endothelial NO PGI2 have been hampered by lack availability suitable cell model. To that end we developed characterized new ovine artery (UAEC)...

To define the role of endothelial nitric oxide (NO) in developmental changes pulmonary vascular resistance and oxygen responsiveness, we determined ontogeny NO production modulation that process arteries from fetal newborn lambs. was assessed by measuring endothelium-dependent arterial guanosine 3',5'-cyclic monophosphate synthesis. Basal rose two-fold late gestation to 1 wk age another 1.6-fold 4 wk. Acetylcholine-stimulated also increased The maturational rise evident at high Po2 vitro, it...

During the follicular phase of ovarian cycle, when local estrogen-to-progesterone ratio is elevated, uterine blood flow elevated. This vasodilatory response reproduced by exogenous 17β-estradiol (E 2 β) administration via a nitric oxide (NO)-mediated mechanism. We hypothesized that endogenous estrogen and E β treatment elevate expression endothelial cell-derived NO synthase (eNOS) in uterine, but not systemic, arteries. Uterine, mammary, systemic (renal and/or omental) arteries were...

Prolonged 17β-estradiol (E 2 β) infusion decreases mean arterial pressure (MAP) and systemic vascular resistance (SVR) while increasing heart rate (HR) cardiac output (CO). It is unclear, however, which beds show increases in perfusion. The purpose of this study was to determine reproductive nonreproductive exhibit alterations blood flow during prolonged E β infusion. Nonpregnant, ovariectomized sheep received either vehicle ( n = 6) or (5 μg/kg iv bolus followed by 6 over 24 h for 10 days;...

Human and ovine pregnancies are associated with increases in plasma levels of estrogens angiotensin II (ANG II), cardiac output (CO), blood volume (BV), uterine flow (UBF), as well attenuated ANG pressor responses. We hypothesized that, nonpregnant animals, prolonged estradiol-17 beta (E2 beta) treatment would reproduce these endocrine hemodynamic alterations. Nonpregnant ovariectomized ewes (n = 5) received 5 microgram E2 beta/kg iv followed by 220 micrograms/day for 14 days. Plasma...

Uterine vasculature is less responsive than systemic to angiotensin II (ANG II)-induced vasoconstriction. We hypothesized that pregnancy augments basal and ANG II-stimulated endothelial prostacyclin (PGI2) and/or nitric oxide (NO) production, which locally increase vascular smooth muscle (VSM) adenosine 3',5'-cyclic monophosphate (cAMP) guanosine (cGMP), respectively. (UA) arteries (SA) from pregnant (P) nonpregnant (NP) sheep were incubated with isobutylmethylxanthine. Basal PGI2, cAMP,...

Estradiol-17β (E 2 β) and its metabolites, which are sequentially synthesized by cytochrome P450s catechol- O -methyltransferase to form 4-hydroxyestradiol (OHE ) 2- 4-methoxestradiol (ME ), elevated during pregnancy. We investigated whether expressed in uterine artery endothelial cells (UAECs) E β metabolites modulate cell proliferation via ER-α and/or ER-β play roles physiological angiogenesis Cultured ovine UAECs from pregnant nonpregnant ewes were treated with 0.1 100.0 nmol/L of β,...