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

1986 ◽  
Vol 250 (5) ◽  
pp. R795-R802 ◽  
Author(s):  
C. E. Wood

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.

1975 ◽  
Vol 80 (1) ◽  
pp. 95-103 ◽  
Author(s):  
Helmut Armbruster ◽  
Wilhelm Vetter ◽  
Rainer Beckerhoff ◽  
Jürg Nussberger ◽  
Hans Vetter ◽  
...  

ABSTRACT In order to investigate the role of renin secretion and of ACTH on the circadian rhythm of plasma aldosterone (PA), plasma renin activity (PRA), plasma cortisol (PC) and PA were determined at short-time intervals in 10 normal supine men. Six subjects were studied under a normal sodium intake and 4 under sodium restriction. In 4 subjects the secretion of ACTH was suppressed by dexamethasone. Under normal sodium intake changes in PA seemed to be more in parallel with changes in PC than by those in PRA as indicated by a higher significant correlation between PA and PC than between PA and PRA in 3 of the 4 subjects. In 1 subject no correlation was observed between PA and PC despite visual synchronism between the plasma concentrations of both hormones. Under dexamethasone medication fluctuations in PA were followed by those in PRA while PC was less than 2 μg/100 ml. In the sodium restricted state, changes in PA were closely paralleled and significantly correlated to PRA while no correlation was seen between PA and PC. Under dexamethasone medication the significant correlation between PA and PRA persisted. Our results indicate that in normal supine man the influence of ACTH and renin on PA may vary with different sodium intakes. Under normal sodium intake ACTH seems to be the dominant factor controlling PA, whereas under sodium restriction changes in PA are mediated through the renin angiotensin system. When the secretion of ACTH is suppressed by dexamethasone, renin controls PA both under normal and low sodium intake.


1977 ◽  
Vol 42 (4) ◽  
pp. 554-558 ◽  
Author(s):  
J. P. Finberg ◽  
G. M. Berlyne

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.


1987 ◽  
Vol 252 (3) ◽  
pp. R624-R627 ◽  
Author(s):  
C. E. Wood

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.


1987 ◽  
Vol 252 (4) ◽  
pp. R743-R748 ◽  
Author(s):  
C. E. Wood

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.


2010 ◽  
Vol 298 (4) ◽  
pp. L575-L583 ◽  
Author(s):  
Sandra Orgeig ◽  
Tamara A. Crittenden ◽  
Ceilidh Marchant ◽  
I. Caroline McMillen ◽  
Janna L. Morrison

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.


1977 ◽  
Vol 43 (3) ◽  
pp. 421-424 ◽  
Author(s):  
J. R. Sutton ◽  
G. W. Viol ◽  
G. W. Gray ◽  
M. McFadden ◽  
P. M. Keane

Responses of plasma renin activity, plasma aldosterone, plasma cortisol, and plasma electrolyte concentration and urinary electrolyte and aldosterone excretion were studied in four men during hypoxic decompression to a stimulated altitude of 4,760 m in a pressure chamber. Three of the four subjects developed significant acute mountain sickness. Plasma sodium and potassium concentrations were unchanged. No significant change in plasma renin activity was observed, but values tended to fall. Plasma aldosterone concentration was depressed while plasma cortisol was elevated and diurnal variation lost. Urinary sodium excretion was unchanged, but urinary potassium and aldosterone excretion were decreased. The decrease in plasma and urinary aldosterone and urinary potassium in the absence of change in plasma renin activity or plasma potassium is of uncertain origin. It is unlikely to be due to a decrease in adrenocorticotropin secretion since plasma cortisol rose during the same time. None of the changes could be causally implicated in the development of acute mountain sickness although the increase in plasma cortisol was greatest in the most ill.


1983 ◽  
Vol 64 (5) ◽  
pp. 463-470
Author(s):  
Y. Takata ◽  
A. E. Doyle ◽  
M. Veroni ◽  
S. G. Duffy

1. Blood pressure, the hypotensive effect of captopril, plasma renin activity, renal renin content and kidney weight were measured in the two-kidney—one-clip model, the one-kidney—one-clip model and the two-kidney—one-clip model with the ureter of the contralateral kidney ligated in rats. The ureteric ligation was performed to abolish urinary excretion from the contralateral kidney in the two-kidney—one-clip model. 2. The development of hypertension after renal artery constriction was earlier and greater in the one-kidney—one-clip model and the two-kidney—one-clip model with ureter of the contralateral kidney ligated than in the two-kidney—one-clip model. A single oral dose of captopril produced a greater fall in blood pressure in both the two-kidney models than in the one-kidney—one-clip group. 3. Plasma renin activity and renal renin content of the clipped kidney were higher in the two-kidney model rats, whether or not the ureter had been ligated, than in the one-kidney—one-clip model animals, although more than half the rats from the two-kidney model had normal values. There was a significant correlation between plasma renin activity and the response to captopril in all groups, whereas in none of the three groups was the correlation between plasma renin activity and blood pressure significant. 4. The clipped kidney had a higher renin content than did the contralateral kidney, and the weight of the ischaemic kidney was decreased compared with the contralateral kidney whether it was untouched or had its ureter ligated. The weight of the clipped kidney was in the order one-kidney—one-clip model > two-kidney—one-clip model with ureter of the contralateral kidney ligated > two-kidney—one-clip model. 5. It was concluded that the renin-angiotensin system was stimulated to the similar degree in some animals for the two-kidney—one-clip models, whether or not the ureter of the contralateral kidney had been ligated, compared with the one-kidney—one-clip animals. This finding suggests that the contralateral kidney can stimulate renin secretion and synthesis in the clipped kidney independently of Na+ excretion.


1985 ◽  
Vol 59 (3) ◽  
pp. 924-927 ◽  
Author(s):  
P. R. Freund ◽  
G. L. Brengelmann

We recently found that paraplegic humans respond to hyperthermia with subnormal increase in skin blood flow (SkBF), based on measurements of forearm blood flow (FBF). Is this inhibition of SkBF a defect in thermoregulation or a cardiovascular adjustment necessary for blood pressure control? Since high resting plasma renin activity (PRA) is found in unstressed individuals with spinal cord lesions and since PRA increases during hyperthermia in normal humans, we inquired whether the renin-angiotensin system is responsible for the attenuated FBF in hyperthermic resting paraplegics. Five subjects, 28–47 yr, with spinal transections (T1-T10), were heated in water-perfused suits. Blood samples for PRA determinations were collected during a control period and after internal temperature reached approximately 38 degrees C. Some subjects with markedly attenuated FBF had little or no elevation of PRA; those with the best-developed FBF response exhibited the highest PRA. Clearly, circulating angiotensin is not the agent that attenuates SkBF. Rather, increased activity of the renin-angiotensin system may be a favorable adaptation that counters the locally mediated SkBF increase in the lower body and thus allows controlled active vasodilation in the part of the body subject to centrally integrated sympathetic effector outflow.


1986 ◽  
Vol 71 (5) ◽  
pp. 613-619 ◽  
Author(s):  
Mr J. K. Evans ◽  
P. F. Naish ◽  
G. M. Aber

1. The effect of oestrone acetate (in total doses of 5 and 10 mg) on systemic and renal haemodynamics and the renin-angiotensin system has been studied in adult female rats. 2. The administration of 10 mg of oestrogen resulted in a significant fall in renal blood flow associated with significant rises in both renal vascular resistance and mean arterial pressure. No changes were noted in cardiac output or total peripheral resistance at either dose. 3. Whilst the higher dose of oestrogen induced a significant increase in plasma renin activity, no change was noted in animals receiving 5 mg of oestrogen. Both regimens caused significant reductions in plasma and intrarenal renin concentrations. 4. Although renal blood flow correlated with plasma renin activity in animals with a normal renal blood flow, no such correlation was noted in animals with oestrogen-induced reductions in renal blood flow. 5. The present study demonstrates that oestrogen-induced reductions in renal blood flow result from a rise in intrarenal vascular resistance which cannot be accounted for by simultaneous changes in either plasma renin activity or renal renin concentration.


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