Bioconversion of arachidonic acid in human pregnant reproductive tissues

Christensen, Niels Juel; Green, K.

doi:10.1016/0006-2944(83)90083-2

Cited by 30 publications

(7 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been suggested (Christensen & Green 1983) that the predominant PGIz production relates to the high vascularity of the myometrium, but similar findings were reported for non-pregnant myometrium (Abel & Kelly 1979) and the myometrial smooth muscle itself has been identified as the main source of the uterine PGIz synthase . While this indicates that, in the uterus, the majority of prostaglandin endoperoxides formed from arachidonic acid are utilized by the PG12 synthase, instead of being directed toward the synthesis of uterotonic prostaglandins, the function of PGIz in the uterus remains unknown.…”

supporting

confidence: 60%

“…Yet, among the many tissues whose contribution to prostaglandin production at parturition has been investigated, the pregnant myometrium itself has received little attention. Moreover, from studies that have been conducted it appears that not a classical prostaglandin, but prostacyclin (PG12) is the main arachidonic acid metabolite in pregnant myometrium (Christensen & Green 1983) be tenfold greater than those of prostaglandin endoperoxide synthase (PGH synthase; also known as cyclo-oxygenase) in this tissue .…”

mentioning

confidence: 99%

See 1 more Smart Citation

Distribution of prostaglandin endoperoxide synthase and prostacyclin synthase in the late pregnant uterus

Moonen¹,

Klok²,

Keirse³

1986

BJOG

View full text Add to dashboard Cite

Summary. Prostacyclin (PGI2) synthase and prostaglandin endoperoxide synthase (cyclo‐oxygenase; PGH synthase) were measured with specific immunoradiometric assays in myometrial microsomes from different areas of a primigravid uterus at 34 weeks gestation. PGH synthase concentrations increased significantly from fundus toward lower segment (P <0·005), but that trend did not apply to PGI2 synthase concentrations, which were significantly higher on the placental than on the non‐placental side of the uterus (P <0·005). PGI2 synthase concentrations showed no further increase with increasing proximity to the placental bed. In myometrium underneath the placental bed there was an inverse relation between the PGH and PGI2 synthase concentrations (r=0·86; P <0·0l) which did not apply to other regions of the uterus. The data suggest that local rather than general mechanisms control uterine PGH and PGI2 synthase concentrations, and that uterine prostaglandin and PGI2 production strongly depend on anatomical relations that have been neglected in previous studies on uterine prostaglandin biosynthesis.

show abstract

supporting

confidence: 60%

mentioning

confidence: 99%

Distribution of prostaglandin endoperoxide synthase and prostacyclin synthase in the late pregnant uterus

Moonen¹,

Klok²,

Keirse³

1986

BJOG

View full text Add to dashboard Cite

show abstract

“…In this preparation there is also the complex peripheral autonomic nervous supply to the paracervical ganglia and uterus described in the review of Papka et al (1987). Furthermore, metabolism of prostaglandins in this in vitro preparation could not be excluded (Christensen 1984).…”

Section: Discussionmentioning

confidence: 99%

“…Uterine tissue has the capacity to synthesize prostaglandins which play a prominent role in the regulation of different uterine functions (Christensen 1984), and also modulate autonomic neurotransmission (Gustafsson 1989 Dissrc ring iind mounting procedures. Animals \\ere stunned and bled.…”

mentioning

confidence: 99%

Influence of prostaglandins and a prostaglandin H synthase inhibitor on cervical secretion of the guinea‐pig

Jonsson

Hammarström

1992

Acta Physiologica Scandinavica

View full text Add to dashboard Cite

The modulatory effects of several prostaglandins and a prostaglandin H synthase inhibitor (indomethacin) on basal as well as nerve stimulation induced secretion from the cervical glands of the guinea-pig were studied. Hypogastric nerve stimulation resulted in a secretory response of +113%. Indomethacin dose dependently inhibited this secretory response. Prostaglandins E2, F2 alpha and I2 inhibited and 19-OH prostaglandin E1 reduced nerve stimulation induced secretion. Prostaglandin I2 and 19-OH PGE1 markedly enhanced basal secretion, while indomethacin as well as PGE2 and PGF2 alpha did not induce any secretion of cervical glands. However, PGF2 alpha in combination with the alpha-adrenergic blocker phentolamine resulted in an increase in secretion. The inhibitory effect of prostaglandins on cholinergic secretory innervation might be due to stimulation of adrenergic nerves exerting an inhibitory influence on cholinergic secretomotor innervation. It is suggested that PGI2 and 19-OH PGE1 exert postjunctional stimulatory effects on the secretory lining and that a lack of secretory effect of PGF2 alpha at least in part may be due to stimulatory effects on adrenergic neurons, inhibiting cholinergic secretomotor transmission. Thus, in this in vitro study it is shown that metabolites of the arachidonic acid cascade and a prostaglandin H synthase inhibitor can modulate cervical secretion and thus maybe influence fertilization.

show abstract

“…Treatment of these diabetic pregnant rats with an alpha-1-adrenoceptor antagonist, nicergoline, re duced significantly these tissular lesions [3] and greatly enhanced the placental blood flow [unpubl. results], whereas it increased hyperglycemia [3], and it has been suggested that the reduction of the placental morpho logical and vascular lesions was, in part, induced by the vasodilatory action of this a r adrenoceptor antagonist [3], Nevertheless, the mechanism whereby nicergoline could exert its vasodilatory action remains un clear, since the placenta is not innervated and lacks ai-adrenoceptors [6,7], Besides, prostanoids which are produced in great amounts by this tissue and act lo cally [8][9][10] are reported to play a major role in the regulation of the uteroplacental blood flow [11][12][13][14][15],…”

Section: Introductionmentioning

confidence: 99%

Influence of an Alpha-1-Adrenoceptor Antagonist, Nicergoline, on Placental Prostanoid Production in Streptozotocin-Induced Diabetic Pregnant Rats

Chartrel¹,

Clabaut²,

Boismare

et al. 1990

Neonatology

View full text Add to dashboard Cite

The aim of this study was to determine if placental prostanoids could mediate the vasodilating action of an alpha- 1-adrenoceptor antagonist, nicergoline (400 μg/kg i.p.), during late pregnancy in streptozotocin-induced diabetic rats (40 mg/kg i.v.). Placental prostanoid concentrations were evaluated by radioimmunoassay. Prostaglandin E₂ levels showed a highly significant increase in diabetic and nondiabetic rats treated with nicergoline (p < 0.001). 6-Keto-PGF_1α concentrations were slightly increased in diabetic rats compared to controls, and this increase was reversed by both nicergoline and insulin treatments. In all groups studied thromboxane B₂ levels were comparable. It is concluded that prostaglandin E₂ could mediate the vasodilating action of nicergoline on the placental irrigation and, therefore, improved the hemodynamic state of this organ in diabetic rats.

show abstract

Bioconversion of arachidonic acid in human pregnant reproductive tissues

Cited by 30 publications

References 24 publications

Distribution of prostaglandin endoperoxide synthase and prostacyclin synthase in the late pregnant uterus

Distribution of prostaglandin endoperoxide synthase and prostacyclin synthase in the late pregnant uterus

Influence of prostaglandins and a prostaglandin H synthase inhibitor on cervical secretion of the guinea‐pig

Influence of an Alpha-1-Adrenoceptor Antagonist, Nicergoline, on Placental Prostanoid Production in Streptozotocin-Induced Diabetic Pregnant Rats

Contact Info

Product

Resources

About