Hypothalamic prostaglandin E2 receptors coupled to an adenylyl cyclase

Wisner, Anne; Bommelaer-Bayet, M. C.; Tiberghien, Christophe; Renard, Claire-Angélique; David, F.; Dray, F.

doi:10.1016/0014-2999(89)90607-9

Cited by 14 publications

(9 citation statements)

References 20 publications

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“…The PGE2 receptor was solubilized from rat brain membrane using a detergent 3-[(3-cholamidopropyl)dimethylammonio]-I -propane sulfonate (CHAPS) (Yumoto et al, 1986) and was found to couple with G,. PGE2 receptor coupled with G, was also demonstrated in the rat hypothalamus (Wisner et al, 1989). A specific binding of PGE2 to bovine adrenal medulla was observed Powell, 1981, 1984).…”

Section: Eicosanoid Receptors and Signal Transductionmentioning

confidence: 88%

Arachidonic Acid Cascade and Signal Transduction

Shimizu

Wolfe

1990

Journal of Neurochemistry

567

346

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Since a review on this topic in this Journal appeared (Wolfe, 1982), the CNS has proved to be a major focus in eicosanoid research. Although our knowledge is limited at the moment, the research in this field is rapidly growing. In this short review, we summarize recent progress of research (1982-1989) in this field with special attention directed to eicosanoid metabolism, functions of eicosanoids in the neuroendocrine system and synaptic transmission, current information on eicosanoid receptors, and the link between eicosanoids and cerebral circulation. Knowledge of the eicosanoids has paved the way to a better understanding of intercellular signal transduction systems, including neuronal functions.

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Section: Eicosanoid Receptors and Signal Transductionmentioning

confidence: 88%

Arachidonic Acid Cascade and Signal Transduction

Shimizu

Wolfe

1990

Journal of Neurochemistry

567

346

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“…We could detect no significant corrclation between changes in thc amount of [3H]PGE, bound to the hypothalamus and its PGE, contcnt. This could result from the existence of two interconvertible forms of the PGE, receptor (18), and from the non-saturating amount of [3H]PGE, used in the binding studies. However, the detected rhythm of [3H]PGE, binding (using 2 nM tritiatcd PGE,) and its relationship to the daily surge of PGE, suggests that it results from the in vivo occupation of the PGE, receptors by endogenous PGs.…”

Section: Discussionmentioning

confidence: 99%

Circadian and Estral Changes in the Hypothalamic Prostaglandin E₂ Content and [³H]Prostaglandin E₂ Binding in Female Rats

Bommelaer-Bayet

Wisner

Renard

et al. 1990

J Neuroendocrinology

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Prostaglandin E, (PGE,) is involved in the luteinizing hormone-releasing hormone-stimulated luteinizing hormone surge in female rats and may act via specific membrane receptors. The following studies were performed to determine whether there were any changes in the hypothalamic PGE, binding and/or PGE, content which were specific to proestrus and not to the rest of the estrous cycle. Groups of female Wistar rats were sacrificed at 3-h intervals throughout the estrous cycle to determine both the circadian and circaestral changes in the hypothalamic PGE, content and [3H]PGE, binding. The hypothalamic PGE, content was maximal at 1700 h on each of the 4 consecutive days of the estrous cycle but was independent of the stage of the cycle.[3H]PGE, binding also displayed a circadian rhythm; the lowest binding occurred near the circadian peak of PGE,, suggesting that the PGE, binding sites were occupied by endogenous PGE,. Since such circadian rhythms were not observed in the hypothalamus of male rats, they may be under the control of ovarian steroids. Also, since PGE, binding and the PGE, content both exhibit a diurnal pattern independent of the day of the cycle, there may be changes in the PGE, receptor-mediated process coupled to an adenylyl cyclase which could explain the luteinizing hormone surge in proestrus.Prostaglandin E, (PGE,) induces the release of Iuteinizing hormone (LH) by stimulating luteinizing hormonc-rclcasing hormone (LHRH) release (1-5). There are also sevcral indications that PGs are involved in the modulation of LHRH release by steroids. The cyclo-oxygenase inhibitor, indomcthacin, prevents the steroidinduced release of gonadotrophin and lowcrs the elevated LH level of castrated animals (6). The preovulatory increase in PGE, synthesis, which precedes the LH surge, indicates that PGE, affects LH release in female rats (7,8), and a peak of PGE, release into the cerebrospinal fluid precedes the LH surge by 20 to 40 min (9). PGE, may act on LHRH release via specific membrane receptors (lo), since specific binding of [3H]PGE, to hypothalamic membranes is correlated with LHRH rclcase in vitro (1 1 ) .The preovulatory LH surge which occurs during proestrus in rats also requires a neural LHRH surge. This, in turn, depends upon adequate circulating titres of ovarian steroids (12). The effect of such a neurogenic stimulus was reported to be dependent on the time of day (1 3). In vitro PGE,-stimulated LHRH release from the median eminence (ME) also depcnds upon the stages of both the estrous and 24-h cycles (14). Such a change in M E sensitivity to PGE, could reflect a modification o f its PGE, binding capacity. However, LHRH release may be differently affected by PGE, and steroids, depending on the area of the hypothalamus: the comparative effect of norepinephrine (N E) on PGE, or LHRH release by the ME alone or hy the ME linkcd to the mediobasal hypothalamus (MBH/ME complex) suggests a regulation of the PGE,-stimulated LHRH release by neurons with cell body located in the MBH (15, 16). Moreover, thc...

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“…Nadler MgSO4 increases the release of PGI2 by cultured human umbilical vein endothelial cells (HUVEC); PGI2 production was two to five times greater when HUVEC were incubated with plasma from preeclamptic patients undergoing MgSO4 therapy than when HUVEC were incubated with pretherapy plasma.36 Also, MgSO4 enhances by 20-36% the prostacyclin liberation from the umbilical cord vascular wall.29 Furthermore, magnesium increases production of prostacyclin or its metabolite 6-keto PGF1(, in other organs, for example cardiac muscle37 and antrum and duodenum. 38 Magnesium increases PGI2 production, decreases PGD2 production,38 and depresses the vascular contractions induced by PGF2 39 There is evidence that magnesium acts directly 40 on the PGF2 (vasodilator) receptor site.…”

Section: Methods and Subjectsmentioning

confidence: 99%

Treatment of severe persistent pulmonary hypertension of the newborn with magnesium sulphate.

Abu-Osba

Galal

Manasra

et al. 1992

Archives of Disease in Childhood

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Eight of nine newborn infants with severe persistent pulmonary hypertension of the newborn (PPHN), and a predicted mortality of 100%, and one infant with a predicted mortality >94% based on alveolar-arterial oxygen tension difference ((A-a)Do2) were treated with magnesium sulphate (MgSO4) as a life saving therapy after they failed to improve with conventional treatment. At high serum concentrations magnesium is a potent vasodilator, muscle relaxant, and sedative. 1 Previous studies showed that magnesium can prevent and reduce hypoxia induced pulmonary hypertension. 1719 Eight infants with severe PPHN and a predicted mortality of 100% and one infant with a predicted mortality >94% based on (A-a)Do2 criteria were treated with magnesium sulphate (MgSO4) as a life saving therapy after they failed to improve with conventional treatment when extracorporeal oxygenation and oscillatory ventilation were not available.Methods and subjects In our unit, newborn infants with PPHN are treated by conventional methods.' 20 Nine infants with a clinical and laboratory picture consistent with PPHN'-3 20 failed to improve with conventional management after a period ranging from 15 to 92 hours (tables 1 and 2). Congenital heart disease was excluded in all infants by echocardiography. (A-a)Do2 was greater than 84-3 kPa (630 mm Hg) in eight of nine infants, and was 82-1 kPa (616 mm Hg) in one infant (table 3). By published criteria all were considered candidates for extracorporeal membrane oxygenation.6 12 (A-a)Do2 was calculated using the following formulas:

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Hypothalamic prostaglandin E2 receptors coupled to an adenylyl cyclase

Cited by 14 publications

References 20 publications

Arachidonic Acid Cascade and Signal Transduction

Arachidonic Acid Cascade and Signal Transduction

Circadian and Estral Changes in the Hypothalamic Prostaglandin E₂ Content and [³H]Prostaglandin E₂ Binding in Female Rats

Treatment of severe persistent pulmonary hypertension of the newborn with magnesium sulphate.

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Hypothalamic prostaglandin E2 receptors coupled to an adenylyl cyclase

Cited by 14 publications

References 20 publications

Arachidonic Acid Cascade and Signal Transduction

Arachidonic Acid Cascade and Signal Transduction

Circadian and Estral Changes in the Hypothalamic Prostaglandin E2 Content and [3H]Prostaglandin E2 Binding in Female Rats

Treatment of severe persistent pulmonary hypertension of the newborn with magnesium sulphate.

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Product

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Circadian and Estral Changes in the Hypothalamic Prostaglandin E₂ Content and [³H]Prostaglandin E₂ Binding in Female Rats