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.

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.

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.

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.

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.

ANTIDIURETIC HORMONE AND CORTICOTROPHIN RELEASE IN MAN

1960 ◽  
Vol 21 (2) ◽  
pp. 171-176 ◽  
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.

Renin, aldosterone, electrolyte, and cortisol responses to hypoxic decompression

1977 ◽  
Vol 43 (3) ◽  
pp. 421-424 ◽  
Author(s):  
J. R. Sutton ◽  
G. W. Viol ◽  
G. W. Gray ◽  
M. McFadden ◽  
P. M. Keane
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Cortisol ◽  
Acute Mountain Sickness ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Plasma Sodium ◽  
Plasma Aldosterone Concentration ◽  
Urinary Potassium ◽  
Mountain Sickness

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.

Seasonal variation in plasma cortisol concentration during pregnancy and the puerperium

1980 ◽  
Vol 8 (5) ◽  
pp. 587-588 ◽  
Author(s):  
JUDITH M. BAKER ◽  
SHEILA L. HANDLEY ◽  
GILL WALDRON ◽  
T. LESLIE DUNN
Keyword(s):  
Seasonal Variation ◽  
Plasma Cortisol ◽  
Cortisol Concentration ◽  
Plasma Cortisol Concentration

Plasma hormonal responses at graded hypohydration levels during exercise-heat stress

1985 ◽  
Vol 59 (6) ◽  
pp. 1855-1860 ◽  
Author(s):  
R. P. Francesconi ◽  
M. N. Sawka ◽  
K. B. Pandolf ◽  
R. W. Hubbard ◽  
A. J. Young ◽  
...  
Keyword(s):  
Body Weight ◽  
Regression Analysis ◽  
Plasma Cortisol ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
O2 Consumption ◽  
Hormonal Responses ◽  
Exercise Period ◽  
Humidity Environment ◽  
Over Time

The effects of graded levels of hypohydration (3, 5, and 7% of body weight) on hormonal responses to exercise in the heat were examined in six heat-acclimated male volunteers. On the day following dehydration, subjects performed light (approximately 25% maximal O2 consumption, 1.03 1 X min-1) exercise in a hot (49 degrees C, 20% relative humidity) environment for four consecutive 25-min intervals interspaced by 10-min rests; blood was obtained before exercise and at approximately 10 min before completion of each exercise period. During euhydration, plasma cortisol (PC) levels manifested significant decrements over time (e.g., time 0, 14.2 micrograms X 100 ml-1 vs. time 2, 8.9 micrograms X 100 ml-1), probably related to its diurnal periodicity. However, during hypohydration, levels of PC were increased and correlated with hypohydration intensity (e.g., time 0, 0, 3, 5, and 7% hypohydration, 14.2, 16.5, 19.8, and 36.2 micrograms X 100 ml-1, respectively). Plasma renin activity (PRA) was increased significantly by hypohydration (e.g., time 0, euhydrated vs. 3%, 3.7 vs. 6.2 units) but was unaffected by exercise in the heat. Plasma aldosterone (ALD) levels were generally increased by exercise in the heat (e.g., time 0 vs. time 4, 3% hypohydration, 12.1 vs. 18.7 ng X 100 ml-1). Regression analysis illustrated that graded intensities of hypohydration were correlated with incremented PRA and ALD through 5% hypohydration. Conversely, PC was incrementally elevated through 7% hypohydration.

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