Effect of arginine vasopressin on regional adrenal blood flow and plasma cortisol concentration in fetal sheep

Pulmonary surfactant is synthesized by type II alveolar epithelial cells to regulate the surface tension at the air-liquid interface of the air-breathing lung. Developmental maturation of the surfactant system is controlled by many factors including oxygen, glucose, catecholamines, and cortisol. The intrauterine growth-restricted (IUGR) fetus is hypoxemic and hypoglycemic, with elevated plasma catecholamine and cortisol concentrations. The impact of IUGR on surfactant maturation is unclear. Here we investigate the expression of surfactant protein (SP) A, B, and C in lung tissue of fetal sheep at 133 and 141 days of gestation (term 150 ± 3 days) from control and carunclectomized Merino ewes. Placentally restricted (PR) fetuses had a body weight <2 SD from the mean of control fetuses and a mean gestational PaO2<17 mmHg. PR fetuses had reduced absolute, but not relative, lung weight, decreased plasma glucose concentration, and increased plasma cortisol concentration. Lung SP-A, -B, and -C protein and mRNA expression was reduced in PR compared with control fetuses at both ages. SP-B and -C but not SP-A mRNA expression and SP-A but not SP-B or -C protein expression increased with gestational age. Mean gestational PaO2was positively correlated with SP-A, -B, and -C protein and SP-B and -C mRNA expression in the younger cohort. SP-A and -B gene expression was inversely related to plasma cortisol concentration. Placental restriction, leading to chronic hypoxemia and hypercortisolemia in the carunclectomy model, results in significant inhibition of surfactant maturation. These data suggest that IUGR fetuses are at significant risk of lung complications, especially if born prematurely.

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CORTISOL SECRETION RATE, GLUCOSE ENTRY RATE AND THE MAMMARY UPTAKE OF CORTISOL AND GLUCOSE DURING PREGNANCY AND LACTATION IN DAIRY COWS

Journal of Endocrinology ◽

10.1677/joe.0.0620371 ◽

1974 ◽

Vol 62 (2) ◽

pp. 371-383 ◽

Cited By ~ 34

Author(s):

J. Y. F. PATERSON ◽

J. L. LINZELL

Keyword(s):

Blood Flow ◽

Milk Yield ◽

Plasma Cortisol ◽

Cortisol Concentration ◽

Secretion Rate ◽

Cortisol Secretion ◽

Entry Rate ◽

Concentration Difference ◽

Plasma Cortisol Concentration ◽

Lactating Cows

SUMMARY Glucose entry rate was measured by primed infusion of [2-3H]glucose, and cortisol secretion rate by infusion of [1,2-3H2]cortisol, in two cows from 142 days before calving to day 287 of lactation. Mammary blood flow and the mammary uptake of glucose and cortisol were also measured. In late pregnancy, cortisol secretion rate was 8·6 ± 3·17 (s.d.) μg/min and plasma cortisol concentration was 1·8 ± 0·52 μg/l. During parturition in one animal the secretion rate was 92 μg/min and plasma cortisol concentration was 15 μg/l. During lactation the secretion rate (26·4 ± 7·14 μg/min) and plasma cortisol concentration (5·6 ± 0·73 μg/l) were significantly greater than in dry cows. The mammary uptake of cortisol was 3 to 4% of the secretion rate in both dry and lactating cows. Glucose entry rate was 5·77 ± 2·250 (s.d.) mg/min/kg0·75 in dry cows and there was no significant mammary uptake of glucose. During lactation the glucose entry increased to 9·45 ± 1·881 mg/min/kg0·75. Mammary uptake of glucose was 3·56 ± 1·949 mg/min/kg0·75. The non-mammary utilization of glucose, glucose entry less mammary uptake, was the same for dry and lactating cows. There was a good correlation between glucose entry and milk yield, and between mammary uptake of glucose and milk yield. Since the mammary arterio-venous glucose concentration difference was relatively constant, it is suggested that the change in mammary blood flow may determine the change in glucose uptake and milk yield.

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Does a decrease in cortisol negative feedback efficacy precede ovine parturition?

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1987.252.3.r624 ◽

1987 ◽

Vol 252 (3) ◽

pp. R624-R627 ◽

Cited By ~ 1

Author(s):

C. E. Wood

Keyword(s):

Sodium Nitroprusside ◽

Negative Feedback ◽

Plasma Cortisol ◽

Feedback Inhibition ◽

Cortisol Concentration ◽

Fetal Sheep ◽

Fetal Plasma ◽

Plasma Cortisol Concentration ◽

Acth Concentration ◽

Vascular Catheters

In sheep and other ruminants parturition is stimulated by increased secretion of fetal cortisol. The mechanism of this increased fetal adrenal activity is not known, but may be dependent on a decreased fetal hypothalamopituitary sensitivity to the negative feedback inhibition by cortisol. Seven fetal sheep (129-142 days gestation), chronically prepared with vascular catheters, were infused with cortisol (10 micrograms/min; n = 5) or vehicle (n = 4) for 5 h. Cortisol infusion increased fetal plasma cortisol to 50.8 +/- 4.3 ng/ml, approximately 33 ng/ml above the corresponding plasma cortisol concentration in the vehicle-infused fetuses. One hour after the end of the cortisol or vehicle infusion, infusion of sodium nitroprusside (50 micrograms/min, iv) increased fetal plasma adrenocorticotropin hormone (ACTH) concentration in both groups of fetuses. Results of another study (15) demonstrated that increases in fetal plasma cortisol of only 1.7 ng/ml for 5 h in younger (117-131 days gestation) fetuses completely blocked the fetal ACTH response to the same dose of nitroprusside. The results indicate that the preparturient rise in fetal ACTH is accompanied by a decrease in cortisol negative feedback.

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Sensitivity of cortisol-induced inhibition of ACTH and renin in fetal sheep

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1986.250.5.r795 ◽

1986 ◽

Vol 250 (5) ◽

pp. R795-R802 ◽

Cited By ~ 6

Author(s):

C. E. Wood

Keyword(s):

Plasma Renin Activity ◽

Plasma Cortisol ◽

Renin Angiotensin System ◽

High Sensitivity ◽

Plasma Renin ◽

Cortisol Concentration ◽

Renin Activity ◽

Fetal Sheep ◽

Fetal Plasma ◽

Plasma Cortisol Concentration

Previous experiments demonstrated that increases in ovine fetal plasma cortisol concentration to maximal stress levels suppressed fetal plasma renin activity and completely inhibited fetal adrenocorticotropin (ACTH) responses to subsequent stress. This study was designed to quantitate the suppressive action of cortisol on both ACTH and renin. Fetal sheep between 117 and 131 days gestation were surgically prepared with chronically implanted catheters. At least 4 days after surgery, vehicle or cortisol (0.25, 0.5, 1, 2, or 3 micrograms/min) were infused for 5 h. One hour after the end of the vehicle or cortisol infusion, fetal ACTH and renin secretion were stimulated by intravenous infusion of sodium nitroprusside. Cortisol infusions suppressed basal plasma renin activity (caused by suppression of plasma renin concentration) to degrees that were related to the increases in fetal plasma cortisol concentration. After cortisol infusions, renin responses to hypotension were apparently suppressed to degrees not obviously related to the rate of cortisol infusion. Fetal plasma ACTH responses to hypotension were completely suppressed by increases in total and unbound fetal plasma cortisol concentration 1.6 and 1.7 ng/ml, respectively. These results demonstrate a high sensitivity of the fetal hypothalamopituitary unit and renin-angiotensin system to cortisol.

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Antenatal glucocorticoids reset the level of baseline and hypoxemia-induced pituitary-adrenal activity in the sheep fetus during late gestation

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00158.2003 ◽

2004 ◽

Vol 286 (2) ◽

pp. E311-E319 ◽

Cited By ~ 21

Author(s):

Andrew J. W. Fletcher ◽

Xiao Hong Ma ◽

Wen X. Wu ◽

Peter W. Nathanielsz ◽

Hugh H. G. McGarrigle ◽

...

Keyword(s):

Hpa Axis ◽

Plasma Cortisol ◽

Acute Stress ◽

Cortisol Concentration ◽

Late Gestation ◽

Dexamethasone Treatment ◽

Fetal Sheep ◽

Plasma Cortisol Concentration ◽

Basal Plasma ◽

Ovine Fetus

This study examined the effects of dexamethasone treatment on basal hypothalamo-pituitary-adrenal (HPA) axis function and HPA responses to subsequent acute hypoxemia in the ovine fetus during late gestation. Between 117 and 120 days (term: ∼145 days), 12 fetal sheep and their mothers were catheterized under halothane anesthesia. From 124 days, 6 fetuses were continuously infused intravenously with dexamethasone (1.80 ± 0.15 μg·kg–1·h–1 in 0.9% saline at 0.5 ml/h) for 48 h, while the remaining 6 fetuses received saline at the same rate. Two days after infusion, when dexamethasone had cleared from the fetal circulation, acute hypoxemia was induced in both groups for 1 h by reducing the maternal fraction of inspired O2. Fetal dexamethasone treatment transiently lowered fetal basal plasma cortisol, but not ACTH, concentrations. However, 2 days after treatment, fetal basal plasma cortisol concentration was elevated without changes in basal ACTH concentration. Despite elevated basal plasma cortisol concentration, the ACTH response to acute hypoxemia was enhanced, and the increment in plasma cortisol levels was maintained, in dexamethasone-treated fetuses. Correlation of fetal plasma ACTH and cortisol concentrations indicated enhanced cortisol output without a change in adrenocortical sensitivity. The enhancements in basal cortisol concentration and the HPA axis responses to acute hypoxemia after dexamethasone treatment were associated with reductions in pituitary and adrenal glucocorticoid receptor mRNA contents, which persisted at 3–4 days after the end of treatment. These data show that prenatal glucocorticoids alter the basal set point of the HPA axis and enhance HPA axis responses to acute stress in the ovine fetus during late gestation.

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ANTIDIURETIC HORMONE AND CORTICOTROPHIN RELEASE IN MAN

Journal of Endocrinology ◽

10.1677/joe.0.0210171 ◽

1960 ◽

Vol 21 (2) ◽

pp. 171-176 ◽

Cited By ~ 2

Author(s):

S. SHUSTER

Keyword(s):

Antidiuretic Hormone ◽

Plasma Cortisol ◽

Cortisol Concentration ◽

Release Factor ◽

Similar Increase ◽

Rapid Infusion ◽

Experimental Procedure ◽

Plasma Cortisol Concentration ◽

Corticotrophin Release Factor ◽

Patients With Diabetes

SUMMARY Plasma cortisol concentrations increased after injections of nicotine. This increase was variable and was no greater than that seen after substitution of normal saline for nicotine. Plasma cortisol concentrations did not increase after nicotine in patients with hypopituitarism and after inhibition of corticotrophin release with triamcinolone. It is concluded that the increased plasma cortisol concentration after injection of nicotine was due to non-specific pituitary stimulation associated with the experimental procedure and not due to any direct effect of the nicotine. Nicotine resulted in a similar increase in plasma cortisol in four patients with diabetes insipidus. Neither rapid infusion of hypertonic mannitol nor ingestion of ethanol had a consistent effect on the plasma cortisol concentration. It is therefore concluded that the antidiuretic hormone is not the 'corticotrophin release factor' in man.

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