Ontogeny of Angiotensin-II-Induced Prolactin Release in vivo and in vitro in Female and Male Rats

Dı́az-Torga, Graciela; Becú-Villalobos, Damasia; Libertun, Carlos

doi:10.1159/000126638

Cited by 13 publications

(11 citation statements)

References 34 publications

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“…It is well known that the sympathetic nerve might stimulate the juxtaglomerular cells in the kidney to release renin which, in turn, elevates the level of angiotensin II in plasma (48,49). Circulating angiotensin II has been described to stimulate prolactin secretion (12) and its potency in stimulating prolactin release from pituitary cells in vitro is one of the highest among potential prolactin-releasing factors (1). Therefore, during hemorrhage the increased circulating angiotensin II acting on pituitary lactotrophs and circulating catecholamines acting on the PO/AH may facilitate prolactin secretion.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, a previous study has shown that the angiotensin II receptor AT 1A is predominantly expressed in the rat forebrain and that, in contrast, the angiotensin II receptor AT 1B subtype predominates in the anterior (21). Although the possibility that angiotensin II functions as a hormone influencing prolactin secretion in certain physiological conditions has been proposed (10,12,13,16,17,21,22) experimental data have not been present. Recently, it has been found that in vivo stimulation of prolactin release by peripherally injected angiotensin II increases with age, and first responses were observed at 20 days of age in both sexes in rats (12).…”

Section: Introductionmentioning

confidence: 97%

“…Although the possibility that angiotensin II functions as a hormone influencing prolactin secretion in certain physiological conditions has been proposed (10,12,13,16,17,21,22) experimental data have not been present. Recently, it has been found that in vivo stimulation of prolactin release by peripherally injected angiotensin II increases with age, and first responses were observed at 20 days of age in both sexes in rats (12). What makes these observations physiologically meaningful are the data indicating that under certain conditions, notably during hemorrhage, angiotensin in plasma reaches levels that are likely to activate prolactin release (11,12,17,20,23,24).…”

Section: Introductionmentioning

confidence: 99%

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Evidence of angiotensin II involvement in prolactin secretion in response to hemorrhage in adrenodemedullated and guanethidine-treated rats

Machado

Reis

Coimbra

2002

European Journal of Endocrinology

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Objective: The present experiments were designed to investigate the influence of the renin -angiotensin system (RAS) on prolactin secretion in response to hemorrhage (1.2 ml/100 g body weight (bw)/2 min). Methods and Results: Male Wistar rats (250 -300 g) were divided into the following experimental groups. (i) Sham-operated animals submitted to intravenous administration of [Sar 1 ,Thr 8 ]-angiotensin II (sarthran), an angiotensin II antagonist (750 ng/100 g bw as a bolus plus an infusion of 25 ng/100 g bw/min over 30 min), which did not alter the prolactin secretion in response to hemorrhage. (ii) Animals submitted to adrenodemedullation which by itself increased the prolactin secretion in response to hemorrhage by 274% ðP , 0:01Þ: However, sarthran infusion into adrenodemedullated rats completely blocked this increased prolactin secretion in response to hemorrhage ðP , 0:01Þ: (iii) Intact animals submitted to blockade of sympathetic noradrenergic pathways by pretreatment with guanethidine (10 mg/100 g bw), which also increased the prolactin secretion in response to hemorrhage by 55% ðP , 0:01Þ: This increased prolactin secretion in response to hemorrhage observed in guanethidine-treated rats was completely blocked by sarthran preinfusion ðP , 0:01Þ: (iv) Adrenodemedullated animals pretreated with guanethidine, which abolished the prolactin secretion induced by hemorrhage. Conclusions: Our data suggest a role for circulating catecholamines in the prolactin secretion response to stress. In addition, the experiments reported here demonstrate that RAS has a stimulatory effect on prolactin secretion in circumstances in which sympathetic activity or adrenomedullary secretion is suppressed. These are the first data demonstrating that a physiological prolactin secretion response to stress depends on the RAS.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Evidence of angiotensin II involvement in prolactin secretion in response to hemorrhage in adrenodemedullated and guanethidine-treated rats

Machado

Reis

Coimbra

2002

European Journal of Endocrinology

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“…Numerous observations indicate that Ang II can contribute to the physiologic regulation of prolactin secretion (Freeman et al 2000), and that it releases prolactin both in vivo and in vitro (Diaz-Torga et al 1994. Angiotensin II receptors, which mediate prolactin secretion (AT1), belong to the family of G protein-coupled receptors.…”

mentioning

confidence: 99%

Dehydroepiandrosterone (DHEA) modulates GHRH, somatostatin and angiotensin II action at the pituitary level

Suárez

Vela²,

García-Tornadú

et al. 2005

Journal of Endocrinology

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In view of the present controversy related to the potential beneficial effects of clinical dehydroepiandrosterone (DHEA) treatments, and considering our own previous results that reveal an influence of this steroid in pituitary hyperplasia development in vivo in rats, we decided to evaluate the role of DHEA in prolactin and GH secretion, as well as in second messengers involved, in cultured rat anterior pituitary cells. DHEA (1 10 5 to 1 10 7 M) did not modify basal GH or prolactin release, and a prolactin inhibitory effect was observed only for androstenediol, a metabolite of DHEA. DHEA partially prevented dopamine (1 10 -6 M)-induced prolactin inhibition and facilitated the prolactin-releasing effect of 10 8 M Ang II, without modifying the resulting Ca 2+ i mobilization. Furthermore, DHEA potentiated the GH release and cAMP production induced by 1 10 8 M GHRH. Finally, DHEA partially reversed the inhibitory effect of 1 10 8 M somatostatin on GH, but not prolactin, release. We conclude that DHEA in vitro, directly or indirectly through conversion into metabolites, is able to modulate the hormonal response of the pituitary to hypothalamic regulators. It can enhance pituitary prolactin release and induce GH secretion. These effects could help explain some of the side effects observed in prolonged DHEA treatments in vivo and should be taken into account when considering its use in human clinical trials.

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“…The anterior pituitary predominantly expresses the AT1B isoform of the AT1 receptor (31,41), with a low expression of the AT1A isoform and the AT2 receptor subtype (41,45). ANG II releases prolactin both in vivo and in vitro (14) and activates extracellular signal-related kinase 1/2 through a calcium-dependent, AT1 receptor-specific mechanism (47). Yet, participation of AT2 receptors in ANG II effects on pituitary function has not been described to date.…”

mentioning

confidence: 99%

Upregulation of angiotensin II type 2 receptor expression in estrogen-induced pituitary hyperplasia

Suárez¹,

Dı́az-Torga²,

González-Iglesias³

et al. 2004

American Journal of Physiology-Endocrinology and Metabolism

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Recent evidence shows that reexpression and upregulation of angiotensin II (ANG II) type 2 (AT2) receptor in adult tissues occur during pathological conditions such as tissue hyperplasia, inflammation, and remodeling. In particular, expression of functional AT2 receptors in the pituitary and their physiological significance and regulation have not been described. In this study, we demonstrate that chronic in vivo estrogen treatment, which induces pituitary hyperplasia, enhances local AT2 expression (measured by Western blot and RT-PCR) concomitantly with downregulation of ANG II type 1 (AT1) receptors. In vivo progesterone treatment of estrogen-induced pituitary hyperplasia did not modify either the ANG II receptor subtype expression pattern or octapeptide-induced and AT1-mediated calcium signaling. Nevertheless, an unexpected potentiation of the ANG II prolactin-releasing effect was observed in this group, and this response was sensitive to both AT1 and AT2 receptor antagonists. These data are the first to document that ANG II can act at the pituitary level through the AT2 receptor subtype and that estrogens display a differential regulation of AT1 and AT2 receptors at this level.prolactin; calcium signaling; Western blot; reverse transcriptasepolymerase chain reaction ANGIOTENSIN II (ANG II) is a key regulator of cardiovascular homeostasis and is also involved in various biological functions, such as hormone secretion, tissue growth, and neuronal activation. Two ANG II receptor subtypes, AT1 and AT2, first distinguished on a pharmacological basis, have been identified by expression cloning from various species, and most biological functions exerted by ANG II are mediated by the AT1 receptor subtype. The AT2 receptor subtype is abundantly and widely distributed in fetal tissues, although its expression is dramatically decreased after birth, being restricted to a few organs such as brain, adrenal, heart, myometrium, and ovary (25,36). Nevertheless, the AT2 receptor is reexpressed in the adult animal under certain pathological conditions, such as ovarian atresia, cardiac and vascular injury, nerve crush, wound healing, and kidney obstruction. AT2 receptors may act as modulators of complex biological programs involved in embryonic development, cell differentiation, tissue protection, and regeneration, as well as in programmed cell death (25, 36).It has been described that all of the components of the reninangiotensin system (RAS) are present in the pituitary and that ANG II is produced locally (13). The anterior pituitary predominantly expresses the AT1B isoform of the AT1 receptor (31, 41), with a low expression of the AT1A isoform and the AT2 receptor subtype (41, 45). ANG II releases prolactin both in vivo and in vitro (14) and activates extracellular signal-related kinase 1/2 through a calcium-dependent, AT1 receptor-specific mechanism (47). Yet, participation of AT2 receptors in ANG II effects on pituitary function has not been described to date.Estrogens can modulate many aspects of the peripheral and pituit...

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Ontogeny of Angiotensin-II-Induced Prolactin Release in vivo and in vitro in Female and Male Rats

Cited by 13 publications

References 34 publications

Evidence of angiotensin II involvement in prolactin secretion in response to hemorrhage in adrenodemedullated and guanethidine-treated rats

Evidence of angiotensin II involvement in prolactin secretion in response to hemorrhage in adrenodemedullated and guanethidine-treated rats

Dehydroepiandrosterone (DHEA) modulates GHRH, somatostatin and angiotensin II action at the pituitary level

Upregulation of angiotensin II type 2 receptor expression in estrogen-induced pituitary hyperplasia

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