Oxytocin at physiological concentrations evokes adrenocorticotropin (ACTH) release from corticotrophs by increasing intracellular free calcium mobilized mainly from intracellular stores. Oxytocin displays synergistic or additive effects on ACTH-releasing factor or arginine vasopressin-induced ACTH secretion, respectively.

Link, H.; Dayanithi, Govindan; Föhr, Karl J.; Gratzl, Manfred

doi:10.1210/endo.130.4.1312449

Cited by 37 publications

(34 citation statements)

References 49 publications

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“…Thus, depletion of intracellular Ca 2 + stores (by the ionophore ionomycin) completely abolished the response of the cells upon oxytocin stimulation. To our knowledge, oxytocin exerts its effect via stimulation of phospholipase-C in the human myometrium (12) and rat pituitary (13,14). A number of other receptors (e.g.…”

Section: Discussionmentioning

confidence: 99%

“…We, therefore, tried to address these points in the present study. We investigated whether activation of oxyto- tin receptors can cause elevations of intracellular free calcium concentrations in human granulosa-lutein cells in a manner similar to that we reported previously in cultured human myometrial cells (12) and rat pituitary corticotrophs (13,14). In addition, we examined the role of oxytocin in progesterone release, and the effect of hCG exerted on the release of oxytocin by cultured human granulosa-lutein cells.…”

Section: Introductionmentioning

confidence: 85%

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Effect of oxytocin on free intracellular Ca2+ levels and progesterone release by human granulosa-lutein cells

Mayerhofer¹

1993

Journal of Clinical Endocrinology & Metabolism

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Oxytocin and its receptor are found in the corpus luteum in a variety of species, including the human.In the present study we used fura- T HE SYNTHESIS of oxytocin in the corpus luteum of the ovary is well established and occurs in a variety of species (l-3; for review, see Ref. 4), including the human (5-8). Moreover, indirect evidence for the presence of oxytocin receptors in human granulosa-lutein cells was provided by a study that showed inhibitory effects of oxytocin on FSHstimulated estradiol secretion (9). Using microdialyzed human corpora lutea, paracrine effects of oxytocin on steroid production were reported. Oxytocin stimulated both progesterone and estradiol release in the young human corpora lutea examined (10). Besides these reports, which give indirect evidence for functional oxytocin receptors in the human ovary, more recently their presence was proven by the detection of oxytocin receptor mRNA in the human ovary (11). However, the signal transduction pathway of the oxytocin receptor in the human corpus luteum has not been examined, and there is no information available concerning whether the expression of oxytocin receptors changes during differentiation. We, therefore, tried to address these points in the present study. We investigated whether activation of oxyto- tin receptors can cause elevations of intracellular free calcium concentrations in human granulosa-lutein cells in a manner similar to that we reported previously in cultured human myometrial cells (12) and rat pituitary corticotrophs (13,14). In addition, we examined the role of oxytocin in progesterone release, and the effect of hCG exerted on the release of oxytocin by cultured human granulosa-lutein cells. Materials and Methods Materials ABSTRACTOxytocin and its receptor are found in the corpus luteum in a variety of species, including the human. In the present study we used fura-2 microfluorimetry to investigate whether activation of the oxytocin receptor of cultured human granulosa-lutein cells causes intracellular calcium (Ca 2 +) signals and affects progesterone release. Although after 1 day in culture, ceHs were not responsive to oxytocin, the number of responsive cells increased steadily during the first 3 days in culture, reaching a maximum on days 4 and 5 (59-66%) and then declined again until day 8. Effective oxytocin concentrations were apparently independent of the culture day, and concentrations as low as 10 nmoljL increased intracellular free Ca 2 + levels from 70-140 nmol/L (basal levels) to maximal peak levels of 800 nmoljL. The oxytocin-induced Ca 2 + signal was not affected by removal of extraceHular Ca 2 + with EGTA. Moreover, depletion of intracellular Ca 2 + stores by ionomycin treatment rendered the cells unresponsive to oxytocin, pointing also at the intraceHular source of the oxytocin-inducible Ca

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 85%

Effect of oxytocin on free intracellular Ca2+ levels and progesterone release by human granulosa-lutein cells

Mayerhofer¹

1993

Journal of Clinical Endocrinology & Metabolism

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“…An alternative interpretation comes from the evidence that in the rat, oxytocin release is activated by diverse acute stressors, including immobilization, ether inhalation and fear-related emotional stress (Lang et al, 1983;Gibbs, 1986;Onaka & Yagi, 1990). Link et al (1992) have shown a synergistic effect of oxytocin and CRF on the release of ACTH at the level of the pituitary, though it is more likely that oxytocin released from the median eminence is involved, rather than that released by the magnocellular system into the general circulation. It is clearly possible, however, that the activation of oxytocin and CRF neurones following CCK administration may be via a common 'stress' pathway.…”

Section: Effect Of Receptor Antagonists On Fos-li In the Brain Followmentioning

confidence: 99%

Involvement of cholecystokinin receptor types in pathways controlling oxytocin secretion

Luckman

Hamamura

Antonijevic

et al. 1993

British J Pharmacology

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1 Intravenous administration of cholecystokinin (CCK) results in a transient activation of oxytocin neurones in the rat, and hence to oxytocin secretion: this activation is followed by expression of c-fos mRNA and of Fos-like immunoreactivity (Fos-LI) in magnocellular oxytocin neurones. Fos-like immunoreactivity is also induced in the regions of the brainstem that are thought to relay information from the periphery to the hypothalamus. 2 Administration of the selective CCKA receptor antagonist MK-329, but not the CCKB receptor antagonist L-365,260, prior to CCK injection, prevented oxytocin release as measured by radioimmunoassay and oxytocin neuronal activation as measured by electrophysiology and by the lack of induction of c-fos mRNA.3 MK-329 abolished the release of adrenocorticotrophic hormone (ACTH) following injection of CCK. 4 MK-329 prevented the expression of Fos-LI in the hypothalamic magnocellular nuclei and in the area postrema and dorsal vagal complex of the brainstem.5 L-365,260 had no effect on the expression of Fos-LI in the brainstem, but attenuated that seen in the hypothalamic magnocellular nuclei. 6 We conclude that CCK acts on CCKA receptors, either in the area postrema or on peripheral endings of the vagus nerve, to cause the release of hypothalamic oxytocin and ACTH. Information may be carried to the hypothalamus in part by CCK acting at CCKB receptors.

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“…The experimental procedures employed in this study have previously been described (21,24) with necessary modifications (6 …”

Section: Perifusion Of Isolated Rat Anterior Pituitary Cellsmentioning

confidence: 99%

“…Pretreatment with I T IS weil established that the secretion of ACTH by anterior pituitary corticotrope cells is stimulated by hypothalamic neurohormones, such as CRF or arginine vasopressin (A VP) (1), and is 5uppressed by adrenal glucocorticoid hormones (2), Severallines of evidence support the notion that oxytocin (OT) is involved in the regulation of pituitary ACTH secrehon; it i5 present in high concentrations in rat hypophysial portal blood (3,4), and high affinity receptors for OT have been identified in the rat pituitary (5). Recently, we have demonstrated that physiological concentrations of OT added in pulsatile fashion to isolated rat pituitary cells stimulate ACTH secretion, independent of other ACTH secretagogues (6). OT may therefore function as a hypophysiotropic hormone contributing to physiological regulation of ACTH release by the hypothalamus.…”

Section: Introductionmentioning

confidence: 99%

Glucocorticoids rapidly inhibit oxytocin-stimulated adrenocorticotropin release from rat anterior pituitary cells, without modifying intracellular calcium transients

Link

1993

Endocrinology

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Glucocorticoid hormones suppress the secretion of ACTH evoked by secretagogues such as CRF and arginine vasopressin. In this study, we investigated the effects of glucocorticoids on ACTH release induced by oxytocin (OT) and on intracellular free calcium ion levels in corticotropes prepared from the adenohypophyses of female Wistar rats.Pulsatile additions of physiological concentration of OT (10 nM) to superfused anterior pituitary cells caused pulsatile ACTH release about 4-fold above basal secretion with similar peak amounts of ACTH du ring subsequent OT pulses. Exposure of the cells to corticosterone (100 nM) or to a selective glucocorticoid receptor agonist RU 28362 (100 nM) for 30 min suppressed OT-stimulated but not basal ACTH release by approximately 60%. Inhibition gradually disappeared during subsequent pulses of OT in the absence of corticosterone. Pretreatment with I

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Cited by 37 publications

References 49 publications

Effect of oxytocin on free intracellular Ca2+ levels and progesterone release by human granulosa-lutein cells

Effect of oxytocin on free intracellular Ca2+ levels and progesterone release by human granulosa-lutein cells

Involvement of cholecystokinin receptor types in pathways controlling oxytocin secretion

Glucocorticoids rapidly inhibit oxytocin-stimulated adrenocorticotropin release from rat anterior pituitary cells, without modifying intracellular calcium transients

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