Regulation of water and solute transport across mammalian plasma cell membranes by prolactin

Shennan, D.B.

doi:10.1017/s0022029900028156

Cited by 15 publications

(4 citation statements)

References 76 publications

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“…One of the least understood actions of prolactin is regulation of solute and water transport across mammalian cell membranes (1602). Studies in this area were motivated by the finding in lower vertebrates that prolactin stimulates solute transport across cell membranes and thus could be an osmoregulatory hormone (153).…”

Section: Osmoregulationmentioning

confidence: 99%

Hypothalamic Prolactin Receptor Messenger Ribonucleic Acid Levels, Prolactin Signaling, and Hyperprolactinemic Inhibition of Pulsatile Luteinizing Hormone Secretion Are Dependent on Estradiol

et al. 2007

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Hyperprolactinemia can reduce fertility and libido. Although central prolactin actions are thought to contribute to this, the mechanisms are poorly understood. We first tested whether chronic hyperprolactinemia inhibited two neuroendocrine parameters necessary for female fertility: pulsatile LH secretion and the estrogen-induced LH surge. Chronic hyperprolactinemia induced by the dopamine antagonist sulpiride caused a 40% reduction LH pulse frequency in ovariectomized rats, but only in the presence of chronic low levels of estradiol. Sulpiride did not affect the magnitude of a steroid-induced LH surge or the percentage of GnRH neurons activated during the surge. Estradiol is known to influence expression of the long form of prolactin receptors (PRL-R) and components of prolactin's signaling pathway. To test the hypothesis that estrogen increases PRL-R expression and sensitivity to prolactin, we next demonstrated that estradiol greatly augments prolactin-induced STAT5 activation. Lastly, we measured PRL-R and suppressor of cytokine signaling (SOCS-1 and -3 and CIS, which reflect the level of prolactin signaling) mRNAs in response to sulpiride and estradiol. Sulpiride induced only SOCS-1 in the medial preoptic area, where GnRH neurons are regulated, but in the arcuate nucleus and choroid plexus, PRL-R, SOCS-3, and CIS mRNA levels were also induced. Estradiol enhanced these effects on SOCS-3 and CIS. Interestingly, estradiol also induced PRL-R, SOCS-3, and CIS mRNA levels independently. These data show that GnRH pulse frequency is inhibited by chronic hyperprolactinemia in a steroid-dependent manner. They also provide evidence for estradiol-dependent and brain region-specific regulation of PRL-R expression and signaling responses by prolactin.

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Section: Osmoregulationmentioning

confidence: 99%

Hypothalamic Prolactin Receptor Messenger Ribonucleic Acid Levels, Prolactin Signaling, and Hyperprolactinemic Inhibition of Pulsatile Luteinizing Hormone Secretion Are Dependent on Estradiol

et al. 2007

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“…PRL is a pleiotropic hormone that influences multiple physiological mechanisms, including gonadotrophin secretion, development of the mammary glands, milk production and maintenance of milk secretion, immune system regulation, and cellular metabolism (Freeman et al 2000). However, one of the least understood actions of PRL is its role in osmotic balance, regulating the transport of solutes and water across mammalian cell membranes (Shennan, 1994).…”

mentioning

confidence: 99%

“…In fish and amphibians, PRL is very important for the maintenance of hydroelectrolytic balance. Studies have indicated that PRL might have an osmoregulatory function in mammalian embryos (Bern, 1975; Shennan, 1994), but the effect of PRL on the hydroelectrolytic balance in higher vertebrates has not been fully clarified. PRL has also been shown to be dramatically affected by different stress stimuli.…”

mentioning

confidence: 99%

Interaction of prolactin, ANPergic, oxytocinergic and adrenal systems in response to extracellular volume expansion in rats

Durlo

Castro²,

Elias³

et al. 2004

Experimental Physiology

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The present study evaluated the effect of acute extracellular volume expansion (EVE) induced by intravenous injection of isotonic (0.15 M NaCl) or hypertonic saline (0.3 M NaCl) on prolactin, corticosterone, vasopressin, oxytocin and atrial natriuretic peptide (ANP) secretion. Male Wistar rats were treated with bromocriptine, sulpiride or dexamethasone. After isotonic and hypertonic EVE, the control group showed a significant increase in the plasma concentrations of prolactin, corticosterone, ANP and oxytocin. The increase in ANP and oxytocin levels in response to hypertonic EVE was more pronounced than to isotonic EVE. Bromocriptine and sulpiride treatments did not modify corticosterone, ANP and oxytocin responses to either isotonic or hypertonic EVE. The increases in prolactin and oxytocin, but not ANP, were blocked in dexamethasone pretreated rats. In conclusion, isotonic or hypertonic EVE induced an increase in the plasma concentrations of prolactin, corticosterone, ANP and oxytocin. The increases in ANP and oxytocin were independent of plasma concentrations of prolactin. The increases in prolactin and oxytocin were blocked by the inhibition of the hypothalamo-pituitary-adrenal (HPA) axis by dexamethasone. However, dexamethasone did not alter the increase in ANP secretion induced by isotonic or hypertonic EVE. Therefore, prolactin might participate in regulation of the hydroelectrolytic balance in mammals; however, in the present study, there was no evidence for direct interaction with ANPergic and oxytocinergic systems. In addition, the responses of prolactin and oxytocin induced by isotonic or hypertonic EVE are modulated by the HPA axis.

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“…The loss of cells via apoptosis may not account for all of the observed weight and protein loss by the corpora lutea. PRL can affect sodium and water transport across the plasma membrane, leading to changes in cell volume [25][26][27]. PRL also alters calcium transport across the plasma membrane [28,29] and has been shown to affect protein synthesis via a calciumdependent system in the corpus luteum [30].…”

Section: Discussionmentioning

confidence: 99%

Repeated Exposure to Prolactin Is Required to Induce Luteal Regression in the Hypophysectomized Rat1

Bowen¹,

Keyes²

2000

Biology of Reproduction

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We investigated whether prolactin (PRL) treatments resembling the intermittent PRL surges of estrous cycles could induce luteal regression in hypophysectomized rats. Immature female rats were stimulated to ovulate and form corpora lutea with exogenous gonadotropins, and were hypophysectomized following ovulation. A single s.c. injection of either vehicle (VEH) or PRL was administered to each rat on post-hypophysectomy Day 8 and again on Day 11. The four resulting treatment groups consisted of rats that received two injections of VEH, VEH followed by PRL, PRL followed by VEH, or two injections of PRL. Rats were killed 24 or 72 h following the second injection. Plasma 20alpha-dihydroprogesterone, luteal weight, and total luteal protein were determined. One ovary was sectioned for immunohistochemistry for monocytes/macrophages, apoptotic nuclei, and major histocompatibility class II (MHC II) molecules. No effect of time (following injection) was observed on any endpoint, indicating that PRL does not have an ongoing regressive action. Time groups from within each treatment group were therefore pooled for analysis. Significant declines (P: < 0.05) in plasma concentrations of 20alpha-dihydroprogesterone, luteal weight, and protein per corpus luteum occurred only after two injections of PRL. Numbers of luteal monocytes/macrophages, apoptotic nuclei, and MHC II-positive cells were low in all groups; numbers of luteal monocytes/macrophages increased following two injections of PRL (P: < 0.05). We conclude that PRL has a cumulative regressive effect on the corpus luteum of the hypophysectomized rat. Drawing a parallel with the estrous cycle, we suggest that continued exposure to PRL, over several cycles, is necessary to induce full luteal regression.

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Regulation of water and solute transport across mammalian plasma cell membranes by prolactin

Cited by 15 publications

References 76 publications

Hypothalamic Prolactin Receptor Messenger Ribonucleic Acid Levels, Prolactin Signaling, and Hyperprolactinemic Inhibition of Pulsatile Luteinizing Hormone Secretion Are Dependent on Estradiol

Hypothalamic Prolactin Receptor Messenger Ribonucleic Acid Levels, Prolactin Signaling, and Hyperprolactinemic Inhibition of Pulsatile Luteinizing Hormone Secretion Are Dependent on Estradiol

Interaction of prolactin, ANPergic, oxytocinergic and adrenal systems in response to extracellular volume expansion in rats

Repeated Exposure to Prolactin Is Required to Induce Luteal Regression in the Hypophysectomized Rat1

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