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Results for “PLACENTAL HORMONES”

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At least 1,045 records · Page 58Linked to original sources
PubMed1986

Rabbit placental relaxin: ultrastructural localization in secretory granules of the syncytiotrophoblast using rabbit placental relaxin antiserum.

Although relaxin has been isolated from the placenta of the human, rabbit, horse, and cat, this study represents the first ultrastructural localization of the hormone in placental tissue. Placentas were removed from rabbits on days 15, 23, and 30 of pregnancy, and the tissues were prepared for light and electron microscopies. The cytoplasm of the syncytiotrophoblast from all stages of pregnancy studied showed positive staining for the hormone at the light level using guinea pig antirabbit relaxin serum and the avidin-biotin technique. Ultrastructurally, the syncytiotrophoblast was found to contain membrane-bounded granules (150-400 nm in diameter) which formed at the Golgi and were seen in close association with the cell membrane. Exocytosis involving the incorporation of the granule membrane into the cell membrane was observed. These granules labeled positively for relaxin after treatment with guinea pig antirabbit relaxin serum and goat antiguinea pig immunoglobulin G-colloidal gold. Control sections in which the relaxin antiserum was absorbed with purified rabbit relaxin or substituted with normal guinea pig serum contained no gold-labeled granules. Cross-reactivity of the rabbit relaxin antiserum with porcine relaxin was demonstrated by labeling of the relaxin-containing granules in the pregnant pig corpus luteum with the rabbit relaxin antiserum and by inhibiting the labeling of rabbit placental and pig corpora luteal granules by absorbing the rabbit relaxin antiserum with porcine relaxin. We have previously described the labeling of rabbit placental relaxin with porcine relaxin antiserum. This study suggests that relaxin is synthesized and secreted from the syncytiotrophoblast of the rabbit placenta, with the subcellular site of storage being membrane-bounded granules.

Animals↗
PubMed2002

Placental buffering of maternal steroid hormone effects on fetal and yolk hormone levels: a comparative study of a viviparous lizard, Sceloporus jarrovi, and an oviparous lizard, Sceloporus graciosus.

We investigated maternal-fetal hormone transfer in the mountain spiny lizard, Sceloporus jarrovi, a viviparous species with a simple chorioallantoic placenta. In one experiment, we examined the effect of elevated maternal progesterone on fetal and yolk hormone levels. Progesterone implants increased maternal progesterone nearly 100-fold; however, the resulting increase in fetal and yolk progesterone was only about 2% of that seen in mothers, providing evidence that the placenta buffers hormone diffusion. In addition, some effects of progesterone treatment differed between male and female fetuses, suggesting that this buffering may differ between the sexes. In a second experiment, we examined the relationship between maternal and fetal hormone levels in viviparous versus oviparous species. We measured endogenous progesterone, testosterone, estradiol, and corticosterone levels in pregnant S. jarrovi and their fetuses and neonates, and in gravid S. graciosus (an oviparous congener) and their fetuses and hatchlings. No clear relationship was identified between maternal and fetal or hatchling S. graciosus hormone levels. However, the data for S. jarrovi suggest that maternal hormones may inhibit perinatal hormone secretion. These findings indicate that, despite the relatively recent evolutionary origin and simple structure of the S. jarrovi placenta, mechanisms for placental mediation of the maternal-fetal endocrine relationship have evolved. Although the placenta appears to buffer hormone transport, maternal hormones can affect fetal and yolk hormone levels, suggesting that disruption of endocrine regulation could be a physiological cost of the evolution of viviparity.

Animals↗
PubMed1994

Corticotropin-releasing hormone-induced vasodilatation in the human fetal placental circulation.

The vasoactive effects of corticotropin-releasing hormone (CRH) in the human fetal-placental circulation in vitro have been investigated. Single lobules of term placentae were bilaterally perfused with constant flows of Krebs' solution (maternal and fetal, 5 ml/min, 95% O2, 5% CO2, 37 degrees C, pH 7.3) and changes in fetal-placental arterial perfusion pressure measured. Effects of human (hCRH) and ovine (oCRH) CRH were examined during submaximal vasoconstriction (100-120 mmHg) of the fetal-placental vasculature induced by prostaglandin F2 alpha (PGF2 alpha), (0.7-2 mumol/L). During infusion of hCRH or oCRH (24-7000 pmol/L) a concentration-dependent vasodilatation was observed. Human CRH and oCRH were equipotent as vasodilator agents (regression analysis; P > 0.05; n = 5). The vasodilator response curves to human and ovine CRH were compared to prostacyclin (PGI2) (1.2-1180 nmol/L). Human and oCRH were 53 times more potent than PGI2 (regression analysis, P < 0.05; n = 5). These results indicate that CRH has powerful vasodilator properties in the human fetal-placental circulation and may play a role in control of placental vascular resistance to blood flow.

Adult↗
PubMedDate not supplied

Placental release of corticotrophin-releasing hormone across the umbilical circulation of the human newborn.

This study attempted to determine the placental release of corticotrophin-releasing hormone (CRH) into the umbilical circulation, and the factors which affect it, by measuring venous and arterial levels for CRH across the umbilical circulation in labouring as well as non-labouring elective caesarean section patients. The relationship with measures of fetal oxygenation and acid-base status at birth was investigated also. Forty-eight patients were studied (term labour n = 30, term elective caesarean section n = 12, and preterm labour n = 6) with blood sampling from a clamped segment of cord after delivery of the fetus and from the cord at its insertion into the placenta after delivery of the placenta, with subsequent measurement of blood gases, pH, base excess, and CRH. For all patients, mean plasma CRH levels in the umbilical and placental vein (115+/-13 and 145+/-18 pg/ml) were higher than those from the corresponding artery (85+/-7 and 102+/-8 pg/ml, P<0.01 and P<0.05, respectively), indicating placental release of CRH into the fetal compartment. In addition, placental venous and arterial cord CRH levels were higher than those from the corresponding umbilical levels (P<0.01 and P<0.02, respectively) indicating continued placental release of CRH into blood within the placenta after clamping of the umbilical circulation and delivery of the fetus. While plasma CRH levels from respective cord vessels were all significantly higher in labouring patients at term versus elective caesarean section patients, there were no differences compared with preterm labouring patients. For all patients, CRH as measured in both the umbilical and placental vein showed a modest inverse correlation to base excess as measured in the umbilical artery, -0.31 and -0.33, respectively, both P<0.05. It is concluded that CRH is released by the placenta into the fetal compartment and is increased with both term and preterm labour, and with metabolic acidosis during labour, supporting a role in the endocrine events of labour and/or compensatory changes in uteroplacental blood flow.

Acid-Base Equilibrium↗
PubMed1994

Short communication: parathyroid hormone-related peptide does not stimulate phosphate placental transport.

It has been demonstrated that parathyroid hormone-related peptide (PTHrP) stimulates calcium (Ca) placental transport. Ca and inorganic phosphorous (P) metabolisms are intimately linked. Thus we have studied the influence of PTHrP on P placental transport in ewes. In our experimental paradigm, synthetic human PTHrP (1-86) fragment intravenously injected in six single chronically catheterized fetuses (3 x 1 micrograms/fetus/day, from day 129 to day 140 of gestation) had no significant effect upon P placental transport which was 131 +/- 6 and 129 +/- 9 mg/kg fetal weight/day in treated and control fetuses, respectively.

Animals↗
PubMed1992

Estrogen negatively regulates rat gonadotropin releasing hormone (rGnRH) promoter activity in transfected placental cells.

To dissect the functional architecture of the rat gonadotropin releasing hormone (GnRH) gene promoter and its regulation by estrogen, gene transfer studies were performed in a placental cell line. 5'-Deletional constructs demonstrated that cis-acting elements important for rGnRH promoter activity in placenta were contained within a region of the proximal promoter between -73 and -16 bp upstream of the transcription initiation site. In addition, an inhibitory region was found from -903 to -424. Deletion of sequences to -424 which removed the inhibitory region, produced a promoter fragment which exhibited a 50% inhibition of GnRH promoter activity in the presence of estrogen (E) and cotransfected estrogen receptor. Negative regulation by E was retained in constructs deleted to -73 bp. We conclude that sequences important for placental cell expression and estrogen regulation of rGnRH lie within the region from -73 to -16. In addition, potential repressor sequences active in placental cells are present between -903 to 424.

Animals↗
PubMed1990

Metabolism and effects of epidermal growth factor and related growth factors in mammals.

The initial observations of Stanley Cohen in the 1960s established that EGF induced in vivo effects such as precocious eyelid opening and tooth eruption. Subsequently the actions of EGF have been extensively explored in cell culture systems. The receptor for EGF was characterized as a prototype model for other growth factors and the now extensive in vitro data indicate multiple functions for EGF. Moreover, EGF and EGF receptors have been characterized in many tissues, and EGF has been identified in most body fluids of several mammalian species. Interestingly, neither EGF antibody administration to newborn animals nor passive immunization of pregnant rodents against EGF has caused major deleterious effects (except the delay in epidermal maturation events), as might be expected from the in vitro studies. This is in contrast to the effects of nerve growth factor antiserum in developing rodents. Also, to date, no pathological EGF deficiency disorder has been characterized. However, the EGF family of growth factors appears to be important in mammalian development and function, although the precise roles and significance are not yet clear. Members of the family may have a role in embryogenesis and fetal growth since receptors have been identified in fetal tissues. Available evidence suggests that TGF alpha subserves the growth factor family roles in fetal development. In the developing postnatal animal pro-EGF mRNA, immunoreactive EGF, immunoreactive TGF alpha, and EGF receptors are present in many tissues. EGF also is produced and secreted by the maternal mammary gland, and mammary derived EGF appears to be important in gut development in the neonatal rodent. There is now extensive data to indicate important hormone-EGF interactions. In the postnatal period, thyroid and steroid hormones including retinoic acid have been shown to modulate EGF and/or EGF receptors in several tissues. GH increases EGF binding in liver and increases urine EGF concentrations. Moreover, EGF stimulates secretion of several hypothalamic and pituitary hormones, increases placental production of hCG and human chorionic somatomammotropin, increases adrenal cortisol production, and inhibits testicular, ovarian, and thyroid hormone secretions. As summarized in this review EGF has been implicated in a number of developmental events including palate and skin differentiation, growth of hair follicles, eye opening and tooth eruption, lung maturation, gut and liver growth, and differentiation of neurons. These EGF actions probably are mediated via autocrine, paracrine, and endocrine routes. A role for salivary and urine EGF in the maintenance of adult stomal, gut, and urinary epithelial surface integrity seems likely, although not yet proven.(ABSTRACT TRUNCATED AT 400 WORDS)

Amino Acid Sequence↗
PubMed1992

Identification and partial purification of serum growth hormone binding protein in domestic animal species.

The chemical nature and variations in serum concentrations of growth hormone binding protein (GHBP) from humans, rabbits, and rodents have been reported. To date little is known about the GHBP of domestic animals. Therefore, we initiated these studies to determine whether a serum GHBP was present in domestic animals and to purify the binding protein (BP) from serum of selected species. Using a dextran-coated charcoal separation assay, specific growth hormone (GH) binding was demonstrated in ovine, bovine, chicken, human, goose, porcine, and equine serum (listed in sequence from lowest to highest binding). Variation in BP activity was relatively high, both within and between species. Yearling ewes had higher serum GHBP than either prepubertal (4 mo) or older (5 yr) ewes. The GHBP was partially purified from chicken, ovine, and porcine serum using GH affinity chromatography. These BP had high affinity (Ka = 2 x 10(8) to 2 x 10(9) L/mol, depending on species) and low capacity (2 x 10(-10) to 5 x 10(-11) mol/unit of protein) for human GH but showed lower binding affinity for homologous GH (Ka = 2 x 10(7) L/mol). The porcine GHBP had the highest and ovine GHBP the lowest affinity for human GH. Other heterologous somatotropic hormones, ovine placental lactogen, and ovine GH displayed higher binding affinity to chicken and pig BP than the respective homologous hormones. Further chromatographic purification of the porcine GHBP resulted in an additional 1,000-fold purification. The estimated molecular weight of porcine GHBP is 50,000 to 60,000 Da. These results demonstrate that the serum from all domestic species tested contains a specific GH-binding moiety and that under the conditions described here human GH is a more efficient ligand than the homologous hormone.

Animals↗
PubMed1981

[Endocrino-pharmacological study of reproduction: Role and biosynthesis of steroid hormones in the feto-placental unit].

Although considerable information is available concerning steroidogenesis in the human fetus, the function of the different steroids formed during pregnancy and the factors regulating this delicate hormones balance are poorly understood. During human pregnancy, the placenta synthesizes large quantities of progesterone, estradiol, estrone and estriol and secretes these hormones into both the maternal and fetal circulations; progesterone from maternal lipoprotein-cholesterol, estradiol and estrone from maternal and fetal dehydroepiandrosterone sulfate (DHAS), and estriol largely from fetal 16 alpha-OH-DHAS. It has been demonstrated that preimplantation blastocysts of several animal species have the capacity to accumulate steroids to pregnenolone to progesterone, and to interconvert estrone and estradiol. Estetrol (E4), 15 alpha-hydroxy derivative of estriol is an interesting compound, since its formation is relatively unique to fetal liver function. Of special interest is that placental sulfatase deficiencies result in an extension of the gestation, and Cesarean section has to be done. This raises the question of the role of estrogens in determining the onset of labor, much as in the case of anencephaly. In general, progesterone may decline prior to an abortion, but there has not been a direct application to clinical practice. Estrogen levels during pregnancy are influenced by factors other than fetal well-being and include fetal weight, placental enzyme function, fetal adrenal function, maternal intestinal flora, maternal renal excretion and maternal liver function. Although not yet extensively utilized, such a dynamic test as the infusion of DHAS may yield useful information within a short period in otherwise complicated cases related to fetal and placental function.

Androgens↗
PubMed1997

Intrauterine programming of hypertension by glucocorticoids.

An ever increasing body of evidence indicates that cardiovascular disease is determined by prenatal experience of undernutrition. Animal experiments suggest that in addition to maternal dietary interventions, exposure of the fetus to glucocorticoid hormones may programme fetal physiology and metabolism, such that cardiovascular functions are permanently altered. Through nutritional regulation of maternal-placental-fetal hormone interactions long term risk of hypertension may be established long before exposure to adult lifestyle factors more usually associated with cardiovascular mortality.

Adaptation, Physiological↗