Catecholamine secretion by the adrenal medulla of the foetal and new‐born foal

Comline, R. S.; Silver, M.

doi:10.1113/jphysiol.1971.sp009546

Cited by 37 publications

(43 citation statements)

References 17 publications

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“…It has also been shown that the innervation of the adrenals is not fully functional until late gestation in these two species (Comline & Silver, 1961, 1966, which would coincide with the apparent increase in adrenocortical sensitivity to ACTH. Events in the foal are also consistent with this hypothesis since the adrenal cortex is unresponsive to ACTH and the innervation of the gland is incomplete until very close to term (Comline & Silver, 1971;. No corresponding information on the development of the splanchnic innervation is as yet available for the fetal pig.…”

Section: Discussionsupporting

confidence: 62%

“…In the present study, a rise in fetal plasma cortisol was observed in response to ACTH released (Lohse & First, 1981). In the foal the main adrenal growth spurt occurs at or even after birth (Comline & Silver, 1971 (Taylor, 1987), the hysterotomy and search for suitable vessels for sampling probably caused some disturbance to placental flow and led to ACTH release. The fetal pituitary is certainly competent from about 0-65 gestation in the lamb and responds to stress with raised ACTH output (Alexander, Britton, Forsling, Nixon & Ratcliffe, 1974).…”

Section: Discussionmentioning

confidence: 77%

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Pituitary‐adrenocortical Activity in the Fetal Pig in the Last Third of Gestation

Silver

Fowden

1989

Exp Physiol

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The responsiveness of the fetal adrenal to a rise in either endogenous or exogenous ACTH (adrenocorticotrophic hormone) was examined acutely in piglets between 70 and 105 days gestation (term, 115 days). In addition the pre-partum changes in plasma ACTH and cortisol were followed in chronically catheterized fetuses and the effect of a continuous intrafetal ACTH infusion on the time of delivery was also investigated. The acute experiments on ten sows were carried out (under sodium pentobarbitone) on twenty-five fetuses, sampled from a branch of the umbilical artery with minimal disturbance. A second sample was taken 10-20 min later after exteriorization or surgery (catheterization). Such fetal manipulation resulted in significant increases in plasma ACTH and cortisol from 70 days gestation and the responses increased with fetal age. No corresponding changes were seen in the controls or in the sow over the same period. An exogenous bolus of ACTH (200 ng ml-' I.v.) evoked rises in fetal plasma cortisol comparable with the endogenous changes (+ 11 + 2 ng ml-', n = 4). Chronic experiments were carried out on fourteen sows catheterized under sodium pentobarbitone anaesthesia at 95-100 days gestation; in fetuses sampled until delivery (at 111-114 days) gradual rises in both fetal plasma cortisol and ACTH were observed. There was a highly significant positive correlation between plasma cortisol and log plasma ACTH (r = 0-81, n = 52, P < 0-001). Analysis of the basal values from the 70-100 day fetuses also showed a positive correlation (r = 0 47, n = 23, P < 0 05) but the slope of the regression line was significantly less than that for the older fetuses indicating a greater adrenocortical response to a given level of ACTH nearer term. In five sows a continuous infusion of ACTH (0' 125 mg day-' for 4-5 days from about 100 days) was given to one or two fetuses per litter (total size, 7-12). This treatment resulted in a rise in fetal plasma cortisol to 85-4 + 8 9 ng ml-', which was equivalent to that found during labour, but did not induce premature parturition.

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Section: Discussionsupporting

confidence: 62%

Section: Discussionmentioning

confidence: 77%

Pituitary‐adrenocortical Activity in the Fetal Pig in the Last Third of Gestation

Silver

Fowden

1989

Exp Physiol

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“…However, group 2 foals showed a significant cortisol response to ACTH, whereas group 1 animals did not despite rising ACTH levels 90-120 min after insulin administration. Adrenocortical sensitivity to endogenous ACTH therefore appears to increase towards term in the fetal foal as is known to occur in response to exogenous ACTH Silver & Fowden, 1994 (Comline & Silver, 1971). The enhanced noradrenaline response to hypoglycaemia observed in group 2, in the present study, may therefore be due, in part, to maturation of the innervation to the fetal adrenal medulla.…”

Section: Discussionsupporting

confidence: 57%

“…In the newborn, insulin-induced hypoglycaemia leads to a dramatic rise in plasma adrenaline with little, if any, change in plasma noradrenaline (Silver et al 1987). Adrenaline is present in the adrenal medulla of the fetal foal during late gestation and can be released in response to asphyxia and direct nerve stimulation under acute conditions in utero (Comline & Silver, 1971). Moreover, the enzyme phenylethanolamine-N-methyl transferase, which converts noradrenaline to adrenaline, is detectable in the fetal adrenal medulla from 250 days of gestation and shows no change in abundance between then and the immediate postnatal period (Han, Fowden, Silver, Holdstock, McGladdery, Ousey, Allen, Rossdale & Challis, 1995).…”

Section: Discussionmentioning

confidence: 99%

“…Increases in the amount of insulin-sensitive tissue towards term may therefore account for the grcater P02 response to insulin observed in the mature fetuses in the present study. Since hypoxia is known to act both centrally and peripherally to stimulate adrenal catecholamine release in the anaesthetized fetal foal (Comline & Silver, 1971), the fall in PO, in group 2 may contribute to the enhanced adrenal responsiveness observed in these fetuses.…”

Section: Discussionmentioning

confidence: 99%

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Sympathoadrenal and other endocrine and metabolic responses to hypoglycaemia in the fetal foal during late gestation

Silver¹,

Fowden²

1995

Experimental Physiology

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SUMMARYIn the present study, ten insulin challenge tests were carried out on nine chronically catheterized fetal foals between 253 and 314 days gestation (term > 320 days). Changes in fetal plasma concentrations of glucose, catecholamines, cortisol, ACTH, free fatty acid (FFA) and lactate were measured before and after a bolus dose of insulin (0-5-2.0 u/kg i.v.). Fetal blood gases, pH, haemoglobin levels and heart rate were measured throughout the 2-3 h experimental period. The fetuses fell into two distinct groups on the basis of proximity to delivery and basal plasma cortisol and catecholamine levels. Those within 2-10 days of delivery after 300 days (group 2, number of experiments (n) = 4) had plasma cortisol and noradrenaline concentrations which were significantly higher (P <0.05) than the corresponding values in fetuses sampled earlier in gestation or at least 2 weeks before foaling (group 1, n = 6). Although insulin administration resulted in a 50% fall in plasma glucose in all animals, group 2 showed significantly greater increases in plasma noradrenaline than group 1. In neither group were there detectable changes in plasma adrenaline. In group 2, increases in plasma cortisol were seen following insulin, whereas no cortisol changes were observed in group 1, despite rises in plasma ACTH. Insulin administration also led to acidosis and increases in heart rate and plasma lactate and FFA levels in all fetuses studied. However, only group 2 became consistently hypoxic during the insulin challenge. No significant changes in plasma glucose or any of the other parameters were observed in the fetuses after saline administration (n = 5). These findings suggest that hypoglycaemia activates the sympathoadrenal system in the fetal foal from 75 % of gestation but has relatively little effect on the fetal pituitary-adrenocortical axis until much closer to term.

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