Endothelial vasodilator production by uterine and systemic arteries. V. Effects of ovariectomy, the ovarian cycle, and pregnancy on prostacyclin synthase expression☆

Magness, Ronald R.; Shideman, Charles R; Habermehl, Deirdre A.; Sullivan, Jeremy A.; Bird, Ian M.

doi:10.1016/s0090-6980(99)00055-6

Cited by 41 publications

(42 citation statements)

References 43 publications

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“…PGIS is distributed in a wide range of tissues including ECs, VSMCs (Nakayama, 2005), and nonvascular SMCs (Magness et al, 2000). Because of the consecutive actions of COX and PGIS, PGI 2 is the main product of AA in vascular tissues.…”

Section: Specific Prostanoid Synthasesmentioning

confidence: 99%

“…Normal pregnancy is an estrogen-and progesteronedominated state characterized by increased cardiac output and uteroplacental blood flow, decreased uterine and systemic vascular resistance, and neovascularization of the uteroplacental vascular bed that is critical for optimum fetal growth and development (Magness et al, 2000). Because the placenta lacks innervation, locally released molecules play a key role in maintaining proper mother-tofetus transfer of nutrients, including oxygen, glucose, and amino acids (Sobrevia et al, 2011).…”

Section: Prostacyclin Metabolism In Pregnancyassociated Vascular mentioning

confidence: 99%

“…Eicosanoid production as well as prostanoids and PGI 2 could also play a role in regulating placental vascular tone and maintaining placental blood flow and nutrient transfer to the fetus. In addition, PGI 2 production by the uterine artery increases 2-to 3-fold in pregnant compared with nonpregnant ewes, probably because of up-regulation of COX1 and PGIS in response to shear stress forces and hormone-dependent mechanisms (Krishnamurthy et al, 1999;Magness et al, 2000). Normotensive pregnant women are refractory to infused vasoactive agents such as angiotensin II, partly as a result of increased synthesis of the vasodilators PGI 2 and PGE 2 (Keith et al, 1993;Krishnamurthy et al, 1999;Magness et al, 2000).…”

Section: Prostacyclin Metabolism In Pregnancyassociated Vascular mentioning

confidence: 99%

“…COX2-deficient mice are infertile because of defects in ovulation, fertilization, and implantation (Loftin et al, 2002a). During pregnancy, COX1 may be more responsible for the increased capacity of uterine artery to produce PGI 2 (Magness et al, 2000). In human term placentas, both COX1 and COX2 mRNA expression are detected, and immunohistochemical staining shows both isoforms in the syncytiotrophoblast layer and in the capillary endothelium within the villi, suggesting a …”

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confidence: 99%

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Molecular Mechanisms Regulating the Vascular Prostacyclin Pathways and Their Adaptation during Pregnancy and in the Newborn

2012

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Section: Specific Prostanoid Synthasesmentioning

confidence: 99%

Section: Prostacyclin Metabolism In Pregnancyassociated Vascular mentioning

confidence: 99%

Section: Prostacyclin Metabolism In Pregnancyassociated Vascular mentioning

confidence: 99%

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confidence: 99%

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Molecular Mechanisms Regulating the Vascular Prostacyclin Pathways and Their Adaptation during Pregnancy and in the Newborn

2012

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“…Prostacyclin, the product of PGIS, is a potent endothelial vasodilator, the level of which is modulated by steroid hormones in the pregnant uterus and the ovarian cycle (30,31). Estrogen modulation of PGIS in the ovary has not been described so far.…”

Section: Discussionmentioning

confidence: 99%

Impact of isotype selective estrogen receptor agonists on ovarian function

Fritzemeier¹,

Hegele‐Hartung²,

Kraetzschmar³

et al. 2004

Exp Clin Endocrinol Diabetes

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Other isotype-selective estrogen receptor (ER) agonists, the selective ER␣ agonist 3,17-dihydroxy-19-nor-17␣-pregna-1,3,5 (10)-triene-21,16␣-lactone and the selective ER␤ agonist 8-vinylestra-1,3,5 (10)-triene-3,17␤-diol, were used in hypophysectomized rats, gonadotropin-releasing hormone antagonist-treated mice, as well as intact rats to elucidate the effects of isotype-selective estrogens on the physiology of folliculogenesis and ovulation. In hypophysectomized rats and gonadotropin-releasing hormone antagonisttreated mice, the ER␤ agonist caused stimulation of early folliculogenesis, a decrease in follicular atresia, induction of ovarian gene expression, and stimulation of late follicular growth, accompanied by an increase in the number of ovulated oocytes similar to 17␤-estradiol (E2). In contrast, the ER␣ agonist had little or no effect on these parameters, implying that direct estrogen effects on ovarian follicular development are mediated by ER␤. In intact rats, E2 and the ER␣ agonist dose-dependently inhibited ovulation, in contrast to the ER␤ agonist. On the other hand, the ER␤ agonist did not stimulate uterine weight in intact rats, in contrast to E2 and the ER␣ agonist. This finding is in line with the assumption that estrogen mediated ovulation inhibition and stimulation of uterine growth are mediated by ER␣ but not by ER␤.pharmacology ͉ folliculogenesis ͉ endocrinology E strogens play a central role in the development and maintenance of female reproductive organs, mammary glands, and sexual behavior. In addition, estrogen's involvement in the function of a number of other tissues such as the bone, the cardiovascular, and the CNS has also been recognized (1, 2).Estrogens exhibit most of their physiological effects through nuclear receptor proteins, the estrogen receptors (ERs). Until recently, it had been assumed that there is only one ER. In 1996, a second ER was detected (3-5), which shares a high degree of homology with the ''classic'' counterpart, specifically in the DNA-and ligand-binding domains. The newly detected receptor is called ER␤, the classic counterpart being renamed as ER␣. The expression pattern of the two ER isotypes is different: ER␤ is predominantly expressed in the ovary and prostate but also other organs not subserving reproduction-related functions. In contrast, its expression is low in the pituitary, the thymus, the uterus, and the liver; these organs express ER␣ at high levels (6, 7). A distinct tissue distribution of ER␣ and ER␤ suggests specific biological functions of ER␣ and ER␤.ER␤ is the predominant ER in ovarian follicles in rodents and nonrodents (8-10). The hypothesis that ER␤ plays an important role in the control of ovarian function is supported by data from various lines of ER␤ knockout mice showing different degrees of female subfertility due to reduced follicular maturation and ovulation rate (11).The stimulatory activity of estrogens on ovarian cell growth, especially folliculogenesis, has been demonstrated in rodent models (12,13). It is suggested that estroge...

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Gap Junction Regulation of Vascular Tone: Implications of Modulatory Intercellular Communication During Gestation

Ampey

Morschauser

Lampe

et al. 2014

Advances in Experimental Medicine and Biology

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In the vasculature, gap junctions (GJ) play a multifaceted role by serving as direct conduits for cell–cell intercellular communication via the facilitated diffusion of signaling molecules. GJs are essential for the control of gene expression and coordinated vascular development in addition to vascular function. The coupling of endothelial cells to each other, as well as with vascular smooth muscle cells via GJs, plays a relevant role in the control of vasomotor tone, tissue perfusion and arterial blood pressure. The regulation of cell-signaling is paramount to cardiovascular adaptations of pregnancy. Pregnancy requires highly developed cell-to-cell coupling, which is affected partly through the formation of intercellular GJs by Cx43, a gap junction protein, within adjacent cell membranes to help facilitate the increase of uterine blood flow (UBF) in order to ensure adequate perfusion for nutrient and oxygen delivery to the placenta and thus the fetus. One mode of communication that plays a critical role in regulating Cx43 is the release of endothelial-derived vasodilators such as prostacyclin (PGI2) and nitric oxide (NO) and their respective signaling mechanisms involving second messengers (cAMP and cGMP, respectively) that are likely to be important in maintaining UBF. Therefore, the assertion we present in this review is that GJs play an integral if not a central role in maintaining UBF by controlling rises in vasodilators (PGI2 and NO) via cyclic nucleotides. In this review, we discuss: (1) GJ structure and regulation; (2) second messenger regulation of GJ phosphorylation and formation; (3) pregnancy-induced changes in cell-signaling; and (4) the role of uterine arterial endothelial GJs during gestation. These topics integrate the current knowledge of this scientific field with interpretations and hypotheses regarding the vascular effects that are mediated by GJs and their relationship with vasodilatory vascular adaptations required for modulating the dramatic physiological rises in uteroplacental perfusion and blood flow observed during normal pregnancy.

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Endothelial vasodilator production by uterine and systemic arteries. V. Effects of ovariectomy, the ovarian cycle, and pregnancy on prostacyclin synthase expression☆

Cited by 41 publications

References 43 publications

Molecular Mechanisms Regulating the Vascular Prostacyclin Pathways and Their Adaptation during Pregnancy and in the Newborn

Molecular Mechanisms Regulating the Vascular Prostacyclin Pathways and Their Adaptation during Pregnancy and in the Newborn

Impact of isotype selective estrogen receptor agonists on ovarian function

Gap Junction Regulation of Vascular Tone: Implications of Modulatory Intercellular Communication During Gestation

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