Negative-feedback inhibition of fetal ACTH secretion by maternal cortisol

1987 ◽  
Vol 252 (4) ◽  
pp. R743-R748 ◽  
Author(s):  
C. E. Wood
Keyword(s):  
Plasma Cortisol ◽  
Feedback Inhibition ◽  
Plasma Renin ◽  
Maternal Plasma ◽  
Cortisol Concentration ◽  
Acth Secretion ◽  
Fetal Plasma ◽  
Plasma Cortisol Concentration ◽  
Subsequent Period ◽  
Arteries And Veins

Previous studies in this laboratory have shown that small increases in fetal cortisol (F) decreased basal fetal plasma renin activity (PRA) and completely inhibited the fetal adrenocorticotropin hormone (ACTH) response to hypotension. The present study was designed to quantitate suppression of fetal ACTH and renin secretion by maternal F. Fetal and maternal femoral arteries and veins were chronically catheterized (11 fetuses, 118-129 days gestation). Maternal intravenous infusion of 0, 0.5, 1.0, and 2.0 micrograms F X kg-1 X min-1 (n = 5-6) increased mean maternal and fetal cortisol and suppressed fetal ACTH responses to a subsequent period of hypotension in a dose-related manner. Increases in fetal plasma cortisol to 8.3 ng/ml completely suppressed the fetal ACTH response to hypotension. The results indicate that increases in maternal plasma cortisol concentration sufficient to produce modest increases in fetal plasma cortisol inhibit fetal ACTH secretion.

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

1987 ◽  
Vol 252 (3) ◽  
pp. R624-R627 ◽  
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.

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

1986 ◽  
Vol 250 (5) ◽  
pp. R795-R802 ◽  
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.

Modification of renin and aldosterone response to heat by acclimatization in man

1977 ◽  
Vol 42 (4) ◽  
pp. 554-558 ◽  
Author(s):  
J. P. Finberg ◽  
G. M. Berlyne
Keyword(s):  
Body Weight ◽  
Plasma Renin Activity ◽  
Plasma Cortisol ◽  
Heat Exposure ◽  
Plasma Renin ◽  
Small Degree ◽  
Cortisol Concentration ◽  
Sweat Loss ◽  
Daily Work ◽  
Plasma Cortisol Concentration

Plasma renin activity (PRA) and aldosterone concentration (PA) increased in eight men following a brief (30--40 min) heat exposure (50 degrees C dry bulb, 25 degrees C wet bulb) with light work. Sweat loss was less than 1% body weight. Plasma cortisol concentration was unchanged or decreased. In four subjects, a standard heat test was repeated in winter and summer (natural acclimatization). The increase in PRA and PA following heat exposure was less in summer than in winter. Four other subjects were artificially acclimated by daily work periods of 90 min at 50 degrees C for 7 days (artificial acclimation). Heat-induced elevation in PRA was considerably reduced by artificial acclimation, although postheat PA was reduced in only two of the four subjects. The small degree of sweat loss under the conditions of these experiments shows that circulating renin and aldosterone levels are increased in the heat even when a significant sodium deficit is not incurred.

Are fetal adrenocorticotropic hormone and renin secretion suppressed by maternal cortisol secretion?

1988 ◽  
Vol 255 (3) ◽  
pp. R412-R417 ◽  
Author(s):  
C. E. Wood
Keyword(s):  
Plasma Cortisol ◽  
Adrenocorticotropic Hormone ◽  
Plasma Concentrations ◽  
Plasma Renin ◽  
Maternal Plasma ◽  
Renin Secretion ◽  
Plasma Acth ◽  
Fetal Sheep ◽  
Fetal Plasma ◽  
Adrenal Secretion

Previous studies from this laboratory have demonstrated that intravenous infusions of hydrocortisone (cortisol) into fetal sheep at rates that produce plasma concentrations achieved during fetal stress inhibit fetal adrenocorticotropic hormone (ACTH) and renin secretion. The present study was designed to test for inhibition of fetal renin and ACTH after maternal adrenal secretion of cortisol. ACTH-(1-24) or saline infusion into 12 pregnant ewes (120-132 days gestation) at rates of 0, 1, 5, or 20 ng ACTH.kg-1.min-1 for 5 h produced dose-related increases in maternal plasma ACTH and cortisol concentrations and fetal plasma cortisol concentration. In the 20-ng.kg-1.min-1 group, increases in fetal plasma cortisol of 8.0 ng/ml (to 24.3 +/- 3.7 ng/ml) did not suppress basal fetal plasma renin activity. One hour after the end of the maternal vehicle or ACTH infusion, fetal ACTH secretion was stimulated by fetal intravenous infusion of sodium nitroprusside. In the 0-, 1-, and 5-ng.kg-1.min-1 groups, fetal ACTH responses to nitroprusside were suppressed in animals infused with ACTH. Together, these results indicate that the maternal adrenal secretion of cortisol inhibits stimulated secretion of ACTH but not renin in 120- to 132-day-gestation fetal sheep.

Effects of increased cortisol concentration on ovine fetal leucine kinetics and protein metabolism

1995 ◽  
Vol 268 (6) ◽  
pp. E1114-E1122 ◽  
Author(s):  
J. R. Milley
Keyword(s):  
Protein Synthesis ◽  
Protein Metabolism ◽  
Plasma Cortisol ◽  
Cortisol Concentration ◽  
Late Gestation ◽  
Fetal Plasma ◽  
Plasma Cortisol Concentration ◽  
Arterial Blood ◽  
Leucine Kinetics ◽  
Ovine Fetal

Fetal protein accretion decreases as gestation progresses, primarily because protein synthesis decreases. Also, glucocorticoid primarily because protein synthesis decreases. Also, glucocorticoid concentrations increase late in gestation, and restraint of growth is one of the most consistently noted effects of glucocorticoids. Therefore, this study was done to determine whether fetal protein accretion is decreased by increased cortisol concentration and whether such an effect might be due to decreased protein synthesis or increased proteolysis. Six days after surgery, fetal leucine and protein metabolism was measured in eight pregnant ewes (114-119 days of gestation) at normal and elevated cortisol concentrations. Arterial blood leucine concentration, fetal leucine disposal rate, and exogenous leucine uptake were unaffected by cortisol infusion. Fetal leucine decarboxylation, however, increased by 19% (P < 0.001). Increased fetal cortisol concentration increased fetal proteolysis by 11% (P < 0.001) but did not affect the use of leucine for protein synthesis. Consequently, fetal protein accretion fell by 34% (P < 0.002). We conclude that increased fetal plasma cortisol concentration increases fetal proteolysis, thereby decreasing the rate of fetal protein accretion, an effect different from the decreased protein synthesis reported in late gestation.

Changes in ovine fetal adrenocortical responsiveness after long-term hypoxemia

1993 ◽  
Vol 264 (5) ◽  
pp. E741-E747 ◽  
Author(s):  
L. M. Harvey ◽  
R. D. Gilbert ◽  
L. D. Longo ◽  
C. A. Ducsay
Keyword(s):  
Arterial Pressure ◽  
High Altitude ◽  
Plasma Cortisol ◽  
Cortisol Concentration ◽  
Plasma Acth ◽  
Fetal Plasma ◽  
Acth Challenge ◽  
Plasma Cortisol Concentration ◽  
Ovine Fetal

This study tested the hypothesis that in the fetus long-term hypoxemia induces premature adrenocortical maturation and augments adrenal responsiveness to adrenocorticotropin hormone (ACTH). Pregnant ewes were exposed to high altitude (3,820 m) from 30 to 120 days gestation, when surgery was performed. Maternal arterial pressure of O2 (PaO2) was maintained at approximately 60 Torr by N2 infusion through a tracheal catheter. Fetal PaO2 was significantly lower in the hypoxemic (21 +/- 0.2 Torr) vs. normoxic (26 +/- 0.4 Torr) fetuses (P < 0.01). Between 125 and 140 days, basal ACTH and cortisol concentrations were similar in both groups. To assess changes in adrenal responsiveness, we challenged the fetuses with ACTH (100 ng/kg body wt, iv bolus) at 126 and 136 days. At 126 days, after ACTH challenge, fetal plasma ACTH peaked at similar values (275 +/- 43 and 250 +/- 26 pg/ml) in normoxic and hypoxemic fetuses, respectively. Plasma cortisol subsequently increased to 84 +/- 8 and 44 +/- 6 ng/ml in these groups. At 136 days, after ACTH challenge, plasma ACTH peaked at 379 +/- 57 and 336 +/- 21 pg/ml in normoxic and hypoxemic fetuses, respectively. Although plasma cortisol concentration in normoxic fetuses increased to 180 +/- 21 ng/ml, levels in hypoxemic fetuses only reached 62 +/- 12 ng/ml (P < 0.05 compared with normoxic). Catecholamine concentrations were not significantly different between the two groups. These data do not support the hypothesis that adrenocortical maturation occurs prematurely, augmenting adrenal responsiveness to ACTH after exposure to long-term hypoxemia. Rather, the ability of the fetus to respond to an ACTH challenge is blunted.

By 94 days of gestation plasma cortisol increases block ACTH response to hypotension in lamb fetuses

1985 ◽  
Vol 249 (4) ◽  
pp. E350-E354
Author(s):  
B. Y. Hargrave ◽  
J. C. Rose
Keyword(s):  
Arterial Pressure ◽  
Plasma Cortisol ◽  
Crossover Design ◽  
Cortisol Concentration ◽  
Plasma Acth ◽  
Fetal Plasma ◽  
Plasma Cortisol Concentration ◽  
Group I ◽  
Group Ii ◽  
Saline Pretreatment

By use of a crossover design, we studied the effects of increasing plasma cortisol concentration on ACTH responses to a standardized stress in 14 lamb fetuses between 94 and 108 days gestation. On a random basis we assigned the animals into two groups of seven. Animals in groups I and II received infusions of cortisol (5 and 1 microgram/min, respectively) or saline for 4 h. After the cortisol or saline pretreatment, we reduced arterial pressure approximately 40-50% in both groups of animals with nitroprusside. After saline pretreatment, hypotension in the group I animals produced an increase in the fetal plasma ACTH from 15 +/- 3 to 200 +/- 20 pg/ml (P less than 0.001), and in the group II animals pretreated with saline plasma ACTH increased from 21 +/- 4 to 141 +/- 19 pg/ml (P less than 0.001) with hypotension. Cortisol pretreatment elevated fetal plasma cortisol levels from 7 +/- 3 to 36 +/- 5 ng/ml in group I and from 8 +/- 4 to 20 +/- 2 ng/ml in group II. The ACTH response to hypotension in both groups was abolished by the cortisol pretreatment. We conclude that by 94 days gestation increases in plasma cortisol within a physiological range block ACTH responses to hypotension in lamb fetuses.

scholarly journals Hyperreninaemic hypoaldosteronism in a dog : case report

1998 ◽  
Vol 69 (1) ◽  
Author(s):  
R.G. Lobetti
Keyword(s):  
Plasma Cortisol ◽  
Plasma Renin ◽  
Cortisol Concentration ◽  
Cortisol Response ◽  
Acth Stimulation ◽  
German Shepherd ◽  
Plasma Cortisol Concentration ◽  
German Shepherd Dog ◽  
Serum Aldosterone ◽  
Basal Plasma

A 9-year-old male German shepherd dog was evaluated for clinical and clinico-pathological changes that were suggestive of Addison's disease. On further investigation the basal plasma cortisol concentration was high, a normal cortisol response to ACTH stimulation occurred, plasma renin activity was elevated and low serum aldosterone concentration was present. A diagnosis of hyperreninaemic hypoaldosteronism was made. Replacement fludrocortisone resulted in complete normalisation of the electrolyte and fluid imbalances. Hyperreninaemic hypoaldosteronism has never been reported in the dog.

Effect of baroreceptor denervation on vasopressin and cortisol responses to angiotensin II infusion in conscious dogs

1989 ◽  
Vol 257 (5) ◽  
pp. R1175-R1181 ◽  
Author(s):  
V. L. Brooks ◽  
C. K. Klingbeil ◽  
E. W. Quillen ◽  
L. C. Keil ◽  
I. A. Reid
Keyword(s):  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Cortisol ◽  
Cortisol Concentration ◽  
Conscious Dogs ◽  
Acth Secretion ◽  
Plasma Cortisol Concentration ◽  
Plasma Vasopressin ◽  
Cortisol Responses

Recent studies suggest that the pressor response to exogenous angiotensin II infusion may, through baroreceptor-dependent mechanisms, counteract the stimulatory effect of the peptide on vasopressin and adrenocorticotropic hormone (ACTH) secretion. To test this hypothesis, the effect of combined cardiac and sinoaortic baroreceptor denervation on the increases in plasma concentrations of vasopressin and cortisol (used as an index of ACTH secretion) produced by angiotensin II infusion was studied in conscious dogs. In eight intact dogs, 30-min angiotensin II infusions at 5, 10, and 20 ng.kg-1.min-1 increased mean arterial pressure from 108 +/- 5 to 126 +/- 5 mmHg, from 101 +/- 4 to 130 +/- 4 mmHg, and from 99 +/- 3 to 138 +/- 4 mmHg, respectively (P less than 0.001). Plasma cortisol concentration increased from 19 +/- 4 to 27 +/- 4 ng/ml, from 19 +/- 4 to 43 +/- 4 ng/ml, and from 19 +/- 4 to 71 +/- 6 ng/ml (P less than 0.01), and plasma vasopressin concentration increased from 2.2 +/- 0.3 to 3.1 +/- 0.3 pg/ml, from 2.3 +/- 0.3 to 3.5 +/- 0.4 pg/ml, and from 2.2 +/- 0.4 to 5.0 +/- 0.5 pg/ml (P less than 0.01). In five to six baroreceptor-denervated dogs, angiotensin II infusion produced increases in mean arterial pressure, plasma vasopressin concentration, and plasma cortisol concentration that were not consistently different from those in the intact dogs. These results demonstrate that baroreceptor denervation does not enhance the vasopressin or cortisol responses to angiotensin II infusion in conscious dogs.

Intrauterine growth restriction delays surfactant protein maturation in the sheep fetus

2010 ◽  
Vol 298 (4) ◽  
pp. L575-L583 ◽  
Author(s):  
Sandra Orgeig ◽  
Tamara A. Crittenden ◽  
Ceilidh Marchant ◽  
I. Caroline McMillen ◽  
Janna L. Morrison
Keyword(s):  
Mrna Expression ◽  
Plasma Cortisol ◽  
Surfactant Protein ◽  
Cortisol Concentration ◽  
Plasma Catecholamine ◽  
Fetal Sheep ◽  
C Protein ◽  
Intrauterine Growth ◽  
Plasma Cortisol Concentration ◽  
The Impact

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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