Hormone Ontogeny in the Ovine Fetus. II. Ovine Chorionic Somatomammotropin in Mid and Late Gestation in the Fetal and Maternal Circulations*

Endocrinology ◽  
1979 ◽  
Vol 104 (6) ◽  
pp. 1828-1833 ◽  
Author(s):  
P. D. GLUCKMAN ◽  
S. L. KAPLAN ◽  
A. M. RUDOLPH ◽  
M. M GRUMBACH
PLoS ONE ◽  
2012 ◽  
Vol 7 (12) ◽  
pp. e52363 ◽  
Author(s):  
Juanita K. Jellyman ◽  
Malgorzata S. Martin-Gronert ◽  
Roselle L. Cripps ◽  
Dino A. Giussani ◽  
Susan E. Ozanne ◽  
...  

2002 ◽  
Vol 283 (1) ◽  
pp. E165-E171 ◽  
Author(s):  
Alison C. Holloway ◽  
David C. Howe ◽  
Gabriel Chan ◽  
Vicki L. Clifton ◽  
Roger Smith ◽  
...  

We hypothesized that urocortin might be produced in the pituitary of the late-gestation ovine fetus in a manner that could contribute to the regulation of ACTH output. We used in situ hybridization and immunohistochemistry to identify urocortin mRNA and protein in late-gestation fetal pituitary tissue. Levels of urocortin mRNA rose during late gestation and were associated temporally with rising concentrations of pituitary proopiomelanocortin (POMC) mRNA. Urocortin was localized both to cells expressing ACTH and to non-ACTH cells by use of dual immunofluorescence histochemistry. Transfection of pituitary cultures with urocortin antisense probe reduced ACTH output, whereas added urocortin stimulated ACTH output from cultured pituitary cells. Cortisol infusion for 96 h in chronically catheterized late-gestation fetal sheep significantly stimulated levels of pituitary urocortin mRNA. We conclude that urocortin is expressed in the ovine fetal pituitary and localizes with, and can stimulate output of, ACTH. Regulation of urocortin by cortisol suggests a mechanism to override negative feedback and sustain feedforward of fetal hypothalamic-pituitary-adrenal function, leading to birth.


1988 ◽  
Vol 254 (4) ◽  
pp. R706-R710 ◽  
Author(s):  
N. D. Ray ◽  
C. S. Turner ◽  
N. M. Rawashdeh ◽  
J. C. Rose

Given the necessity of the adrenal gland in maintaining cardiovascular function in adults of various species, these experiments were conducted to determine if fetal bilateral adrenalectomy results in altered resting heart rate, hypotension, and decreased basal blood volume as well as a diminished ability of the fetus to maintain arterial pressure and restore blood volume in response to hemorrhage. We studied heart rate, arterial blood pressure, and blood volume changes in response to hemorrhage of 20% of blood volume at 2%/min in seven adrenalectomized and six intact chronically cannulated unanesthetized lambs between 119 and 133 days of gestation. Blood volumes and percent restitution of shed volume were determined using 51Cr-tagged red blood cells and changes in hematocrit. There was no significant difference between groups in basal heart rate, mean arterial pressure, hematocrit, and blood volume. The two groups were similar to hemorrhage-induced changes in these and restitution of volume. Therefore, fetal adrenal glands are not necessary for basal cardiovascular function or regulation subsequent to moderate hemorrhage in the late gestation ovine fetus.


2019 ◽  
Vol 97 (Supplement_3) ◽  
pp. 244-244
Author(s):  
Hanaa Mansour ◽  
Caleb O Lemley ◽  
Russell Anthony ◽  
Kendall C Swanson ◽  
Anna T Grazul-Bilska ◽  
...  

Abstract Melatonin plays a role as a vasodilator. Vasoactive and angiogenic factors are expressed by placental binucleate cells (BNC) and produce chorionic somatomammotropin (CSH), known to impact fetal and placental growth. We hypothesized that melatonin supplementation and restricted nutrition from mid- to late-gestation would alter CSH concentration and some characteristics of BNC in placenta. At day 50 of gestation, ewes carrying singletons were randomly assigned to a 2 × 2 factorial design and were fed either an adequate (ADQ; 100% NRC; n = 15) or restricted (RES; 60% NRC; n = 15) diet supplemented with 0 (CON, n = 14) or 5 mg of melatonin (MEL; n = 16). Placentomes were collected on day 130 of gestation and preserved in formalin for histological analysis. Cotyledon (COT) were snap frozen for western immunoblotting analyses. Tissue sections were stained using biotinylated Dolichos Biflurus (DBA; a marker of fetal membrane) lectin and fluorescein labeled Texas red-avidin and fluorescein labeled Griffonia Simplifolica (BS) lectin (a marker of BNC). The number, area, and diameter of BNC in COT were determined by image analysis. For immunoblotting, protein was extracted from COT in SDS phosphate buffer, loaded equally, and separated on 12.5% polyacrylamide gels. Protein was transferred to PVDF membranes and incubated with rabbit anti-CSH. Bands were visualized and imaged. Data were analyzed using Proc Mixed procedure of SAS. Melatonin supplementation and restricted nutrition did not affect BNC number, area, or diameter, or CSH protein expression. While we reject our hypothesis that melatonin supplementation and nutrient restriction would alter the CSH concentration and BNC characteristics in COT, we continue to evaluate if the BNC produce angiogenic or vasoactive factors that may influence placental and mammary gland functions in sheep.


1998 ◽  
Vol 275 (2) ◽  
pp. R357-R362 ◽  
Author(s):  
Kirsten R. Poore ◽  
I. Ross Young ◽  
Benedict J. Canny ◽  
Geoffrey D. Thorburn

Maturation of the fetal adrenal gland is critical for the onset of ovine parturition. It has long been proposed that the fetal adrenal gland may be under inhibitory influences during late gestation. In vitro evidence has suggested that angiotensin II may be such an inhibitory factor and may help to prevent a premature increase in cortisol concentrations. The aim of this study was to test the effect of angiotensin II infusion in vivo on basal cortisol concentrations and fetal adrenal responsiveness to an ACTH-(1—24) challenge. Fetuses received a continuous infusion of either angiotensin II (100 ng ⋅ min−1 ⋅ kg−1; n = 7) or saline (2 ml/h; n = 4), which commenced at 140 days of gestation (GA) and continued for a total of 50 h. Adrenal responsiveness to the administration of ACTH-(1—24) (5 μg/kg) was determined during angiotensin II or saline infusions at both 2 and 48 h after infusion onset. Angiotensin II had no significant effect on adrenal responsiveness after acute (2 h) or chronic (48 h) infusion. There was no effect of saline or angiotensin II infusion on basal immunoreactive ACTH or cortisol concentrations after 2 h, but there was a significant increase in basal cortisol concentrations in both treatment groups by 48 h, probably reflecting the normal rise in cortisol concentrations at this GA. Mean arterial blood pressure was significantly increased in angiotensin II-infused fetuses only. This study has therefore found no evidence to suggest that angiotensin II infusion in vivo modulates fetal basal cortisol concentrations or adrenal responsiveness in the last week of gestation, in contrast with previous in vitro studies. These results throw into question the proposed role of angiotensin II as a negative modulator of adrenal function in the ovine fetus.


Neonatology ◽  
2015 ◽  
Vol 107 (4) ◽  
pp. 249-255 ◽  
Author(s):  
Eileen I. Chang ◽  
Charles E. Wood
Keyword(s):  

1986 ◽  
Vol 109 (3) ◽  
pp. 307-312 ◽  
Author(s):  
N. S. Bassett ◽  
P. D. Gluckman

ABSTRACT The ontogenesis of the pulsatility of GH in the ovine fetus was determined by obtaining blood samples at 20-min intervals for 3-h periods from fetuses (n = 33) at various stages of development (76–147 days gestation), and in neonatal life (n = 19). A significant increase (P <0·01) in the GH mean, nadir and maximum, and pulse height was observed between the ages of 100 and 130–139 days of gestation. An analysis of the difference in the mean, maximum and nadir concentrations between 100 and 139 days of gestation revealed that males had higher GH levels than females (P <0·05). There was a significant fall in plasma GH concentrations from 140 days of gestation to term, but before the onset of active labour. There was a more rapid fall in the circulating levels of fetal GH directly following birth. Immediately before birth fetal GH levels were still relatively high, but within 60 min of birth they had fallen by more than 80%. It is suggested that these changes in the pulsatile pattern of GH release are a consequence of both maturational changes in the hypothalamic-pituitary unit and the effects of pregnancy-related factors on GH release. The sexually dimorphic nature of GH release in the adult is also observed in the sheep fetus during late gestation. J. Endocr. (1986) 109, 307–312


1997 ◽  
Vol 9 (8) ◽  
pp. 767 ◽  
Author(s):  
Kelly J. Crossley ◽  
Marcus B. Nicol ◽  
Jonathan J. Hirst ◽  
David W. Walker ◽  
Geoffrey D. Thorburn†

The high rate of progesterone synthesis by the placenta in late gestation exposes the ovine fetus to high concentrations of progesterone and its metabolites that may affect activity of the fetal brain. The aim of this study was to determine the effect of inhibiting maternal progesterone synthesis on sleep–wake activity in fetal sheep. Fetal and maternal vascular catheters, a fetal tracheal catheter, and electrodes for recording fetal electrocortical (ECoG), electro-ocular (EOG) and nuchal muscle electromyographic (EMG) activity were implanted. At 128–131 days gestation, progesterone production was inhibited by an injection of trilostane (50 mg), a 3β-hydroxysteroid dehydrogenase inhibitor. Vehicle solution or progesterone (3 mg h -1 ) was then infused into the ewe between 6 and 12 h after the trilostane treatment. Maternal progesterone concentrations were significantly reduced from 1–24 h after trilostane treatment (P < 0·05) when followed by vehicle infusion. Fetal breathing movements (FBM), EOG, nuchal muscle EMG, and behavioural arousal increased 12 h after trilostane treatment (P < 0 · 05). In contrast, there was no change in fetal arousal, EOG, EMG or FBM activities when progesterone was infused after the trilostane treatment. These findings show that progesterone can influence fetal behaviour, and indicates that normal progesterone production tonically suppresses arousal, or wakefulness in the fetus.


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