Further evidence for the role of prolactin on human fetoplacental osmoregulation

Leontic, E; Schruefer, John J.; Andreassen, B.; Pinto, Humberto; Tyson, John E.

doi:10.1016/0002-9378(79)90067-x

Cited by 47 publications

(16 citation statements)

References 9 publications

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“…Osmoregulatory effect of prolactin have also been found in the chick embryo (Doneen and Smith 1982 ;Murphy et al 1986), and in the transport of water across the human amnion (Leontic and Tyson 1977 ;Leontic et al 1979). The increased speed of embryonic development with prolactin reported here may be related to the same osmoregulatory effect.…”

Section: Discussionsupporting

confidence: 72%

Improvement of mouse embryo development in vitro by prolactin.

Yohkaichiya

Fukaya

Hoshiai

et al. 1988

Tohoku J. Exp. Med.

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Section: Discussionsupporting

confidence: 72%

Improvement of mouse embryo development in vitro by prolactin.

Yohkaichiya

Fukaya

Hoshiai

et al. 1988

Tohoku J. Exp. Med.

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“…Prolactin and renin have been associated with salt and water balance during pregnancy [16][17][18][19][20], and decidual prolactin has also been implicated in the production of surfactant in the fetus [21][22][23]. Prolactin has been found to inhibit PGE 2 production by the amnion [24]; therefore the inhibition of prolactin may be involved in the pathogenesis of preterm labor.…”

Section: Discussionmentioning

confidence: 99%

Lipopolysaccharides Inhibit Prolactin and Renin Release from Human Decidual Cells1

Chao

Poisner

et al. 1994

Biology of Reproduction

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Human decidual tissue consists of a heterogeneous population of cells, including stromal cells, lymphocytes, and macrophages. Lipopolysaccharides (LPS), which bind to specific cell surface receptors on macrophages, have been shown to increase prostaglandin production by the decidua and amnion. To determine whether LPS may also affect decidual hormone production, we have examined the effects of LPS on the synthesis and release of prolactin and renin. Dispersed cells from term decidual tissue exposed to LPS L2880 (Escherichia coli, 1 microgram/ml) released significantly less prolactin and renin than control cells after 24 h of exposure. Maximal inhibition of prolactin (31.6%) and renin (62.5%) release was noted at 72 and 96 h of exposure, respectively (p < or = 0.0002 in each instance). The inhibition of prolactin and renin release was dose-dependent, with half-maximal inhibition at a dose of approximately 10 ng/ml. LPS caused a decrease in prolactin synthesis as well as release. In addition, LPS inhibited the stimulation of prolactin release in response to insulin, a known secretagogue of prolactin release. After 24, 48, and 72 h of exposure, the magnitude of the stimulation of prolactin release by cells exposed to insulin (100 ng/ml) in the presence of LPS (1 microgram/ml) was 84.5, 57.5, and 35.2% less, respectively, than that of cells exposed to insulin alone (p = 0.0001 in each instance). LPS L6011 (Salmonella endotoxin) also inhibited prolactin and renin release. LPS had no effect on overall protein or DNA synthesis and did not cause release of alkaline phosphatase and lactate dehydrogenase.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…Although an agreement is far from being reached [Adler et al, 1975;Berl et al, 1976;Epstein et al, 1977;Dearlove, 1981;Bliss and Lote, 1982], several reports have proposed an association between PRL and osmoregula tion, the hormone being osmotically regu lated [Buckman and Peake, 1973;Buckman et al, 1973;Relkin, 1974;Andersen et al, 1982] , or acting on osmotic regulation [Dharmamba et al, 1967;Josimovich et al, 1977;Ensor, 1978;Leontic et al, 1979;Gopalakrishnan et al, 1980;Mor ley et al, 1981]. Since loss of endogenous heat generated by contracting muscles can lead to marked blood fluid shifts [Senay, 1979], we postu lated that prolactinemic changes observed during exercise could be associated with vari ations in core temperature and/or in blood osmolality.…”

Section: Introductionmentioning

confidence: 99%

Exercise-Induced Blood Prolactin Variations in Trained Adult Males: A Thermic Stress More than an Osmotic Stress

Brisson¹,

Audet

Ledoux

et al. 1986

Horm Res

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Blood prolactin (PRL) variations have been linked to temperature and osmotic changes in several species. The latter factors are here explored to better understand blood PRL responses frequently induced during physical exercise. Since body heat generated by exercise can lead to marked body fluid shifts, it was postulated that PRL changes observed during exercise could be associated with variations in body temperature and/or blood osmolality (OSM). A wide range (38.5–40.5°C) of rectal temperatures (Tr; used here to appreciate core temperatures) were theoretically selected and randomly assigned as targets to male runners. Measured by thermistor probe, target Tr were obtained by a combination of factors: (a) ↑ heat production by treadmill running, and (b) ⇓ heat losses by appropriate clothing (⇓ evaporation) in warmed (⇓ radiation) and hypo ventilated (⇓ convection) laboratory conditions. For each subject, target Tr was attained not prior to 30 min after initiation of running, and had to be maintained for at least 10 min, for a mean ( ± SD) running time of 52.6 ± 10.0 min. In a first protocol, hypohydration was provoked in 26 runners (23.9 ± 4.7 years) by total restriction of water intake. In a second protocol (10 different runners: 22.3 ± 3.3 years), euhydration was maintained by water intake (20 ml/kg body weight). Venous blood was sampled at rest before and immediately after the run. PRL was assayed by RIA; OSM was measured by freezing point depression; sodium was analyzed by flame photometry. At rest, before the heat-producing exercise, mean PRL values were 9.4 ± 3.4 ng/ml for both eu/hypohydrated groups. In the hypohydrated runners, exercise-induced hyperthermia was significantly (r = 0.82; p < 0.0005) associated with blood PRL responses. Moreover, these changes in Tr were also significantly (r = 0.54; p < 0.0025) related to changes in OSM, the latter variations being mostly explained (78 %) by the accompanying hypernatremia. In the euhydrated group of runners, the hyperthermic exercise failed to induce significant changes in OSM (r = 0.22; p > 0.15) and, as expected, variations in blood sodium levels were also not significant under these conditions. However, hyperthermic running in these iso-osmolar conditions did not prevent blood PRL levels from rising (r = 0.77; p < 0.0005). It was thus concluded that, in male trained runners, exercise-induced blood PRL responses could be derived more from thermic than from osmolar stresses.

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Further evidence for the role of prolactin on human fetoplacental osmoregulation

Cited by 47 publications

References 9 publications

Improvement of mouse embryo development in vitro by prolactin.

Improvement of mouse embryo development in vitro by prolactin.

Lipopolysaccharides Inhibit Prolactin and Renin Release from Human Decidual Cells1

Exercise-Induced Blood Prolactin Variations in Trained Adult Males: A Thermic Stress More than an Osmotic Stress

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