FAMILIAL ADRENOCORTICAL HYPOPLASIA WITH EARLY CLINICAL AND BIOCHEMICAL SIGNS OF MINERALOCORTICOID DEFICIENCY (HYPOALDOSTERONISM)

1977 ◽  
Vol 84 (3) ◽  
pp. 605-619 ◽  
Author(s):  
Knud E. Petersen ◽  
Inge Tygstrup ◽  
Erik Thamdrup
Keyword(s):  
Sodium Chloride ◽  
Plasma Renin Activity ◽  
Leydig Cells ◽  
Adrenal Glands ◽  
Plasma Renin ◽  
Cortisol Secretion ◽  
Fat Tissue ◽  
Histological Changes ◽  
Corticosterone Secretion ◽  
Adrenal Hypoplasia

ABSTRACT Biochemical investigations in a boy with a salt losing syndrome revealed a very low secretion of aldosterone which did not rise during salt deprivation, in spite of a normal rise in plasma renin activity. Cortisol secretion was normal - but subsequently decreased, while the corticosterone secretion was high. The patient was studied at the age of 5 weeks, 3 months and also at the age of 8 months. He survived until the age of 18 months on treatment with sodium chloride and DOCA, but did not receive glucocorticoids. At autopsy the adrenal glands were absent, but in fat tissue from the upper renal poles foetal adrenal cortex tissue was found. The histological picture agrees well with other cases which could be designated as "foetal-cortex-only" adrenal hypoplasia. The same histological changes were demonstrated in the boy's brother who died suddenly at the age of 6 weeks. The boy's testes were advanced in maturation to a stage of about ten years: spermatocytes and Leydig cells were present.

PLASMA RENIN ACTIVITY IN CONGENITAL VIRILIZING ADRENAL HYPERPLASIA

PEDIATRICS ◽  
1968 ◽  
Vol 41 (5) ◽  
pp. 897-904
Author(s):  
Masashi Imai ◽  
Yoshio Igarashi ◽  
Hirofumi Sokabe
Keyword(s):  
Sodium Chloride ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Adrenal Hyperplasia ◽  
Peripheral Plasma

Peripheral plasma renin activity was markedly elevated in two cases of the salt-losing form of congenital virilizing adrenal hyperplasia. The renin activity was reduced after treatment with deoxycorticosterone and sodium chloride. In the hypertensive form of the plasma renin activity was suppressed.

Urinary kallikrein and systemic prostacyclin synthesis during sodium chloride infusion in normal man

1985 ◽  
Vol 68 (5) ◽  
pp. 537-543 ◽  
Author(s):  
M. L. Watson ◽  
A. D. Cumming ◽  
A. T. Lambie ◽  
J. A. Oates
Keyword(s):  
Sodium Chloride ◽  
Plasma Renin Activity ◽  
Plasma Protein ◽  
Sodium Excretion ◽  
Protein Concentration ◽  
Plasma Renin ◽  
Urine Flow ◽  
Renin Activity ◽  
Urinary Kallikrein ◽  
Plasma Protein Concentration

1. An intravenous infusion of 3 litres of sodium chloride solution (saline: 150 mmol/l) was given over 1 h to normal subjects. 2. During and immediately after the infusion, renal plasma flow increased in the majority of subjects, but the rise was not statistically significant. Significant increases in urine flow, sodium excretion, urinary kallikrein excretion and urinary excretion of dinor-6-keto prostaglandin (PG) F1α, a measure of systemic PGI2 synthesis, were noted. Plasma renin activity and plasma protein concentration were significantly lowered by the infusion. 3. At 2 h after the end of the infusion, although urine flow fell significantly, sodium excretion had not decreased. The reduction in plasma renin activity and plasma proteins persisted, and excretion of kallikrein and the PGI2 metabolite returned to control values. 4. Overall, urinary kallikrein excretion correlated significantly with urine flow and with sodium excretion. Peak kallikrein excretion occurred in the second 30 min of the infusion, and preceded maximal urine flow and sodium excretion. 5. The results suggest that increased systemic synthesis of PGI2 occurs in response to an acute infusion of sodium chloride, and may be an adaptive response of the vasculature to volume expansion. They support a role for the renal kallikrein-kinin system in the early diuretic and natriuretic response to saline infusion; the reduction in plasma renin activity and plasma protein concentration may be involved in both the early response and the persistent natriuresis 2 h after the infusion.

Effects of an acute calcium load on plasma ACTH, cortisol, aldosterone and renin activity in man

1984 ◽  
Vol 105 (2) ◽  
pp. 251-257 ◽  
Author(s):  
Roland Isaac ◽  
Jean-Paul Raymond ◽  
Muriel Rainfray ◽  
Raymond Ardaillou
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Cortisol Secretion ◽  
Plasma Acth ◽  
Aldosterone Secretion ◽  
Cortisol Responses ◽  
Calcium Load

Abstract. Plasma adrenocorticotrophin (ACTH), cortisol and aldosterone increased during and after iv administration of calcium gluconate in 4 normal subjects, one patient with hypoparathyroidism and one patient with hypothyroidism. On the other hand, there was a decrease in plasma renin activity but only in the normal subjects. Plasma ACTH and cortisol responses to calcium were abolished whereas plasma aldosterone response persisted in 2 normal subjects pre-treated with dexamethasone. The results observed after calcium administration were compared to those observed after infusion of the solvent only in 6 normal subjects and 4 thyroidectomized patients who were studied twice at 3 day intervals. Plasma ACTH, cortisol and aldosterone were higher when calcium was administered. Plasma renin activity was not statistically different whether or not calcium had been injected in the subjects studied twice. These results demonstrate a direct effect of calcium on ACTH and aldosterone secretion which is not mediated by calcitonin and parathyroid hormone. The stimulatory effect of calcium on cortisol secretion depends on the increase in plasma ACTH.

Decreased Plasma Renin Activity and Renin Release in Rats with Phaeochromocytoma

1977 ◽  
Vol 53 (5) ◽  
pp. 447-452
Author(s):  
J. C. S. Fray ◽  
P. V. H. Mayer
Keyword(s):  
Sodium Chloride ◽  
Plasma Renin Activity ◽  
Perfusion Pressure ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Release ◽  
High Sodium ◽  
Sodium Chloride Loading ◽  
And Control ◽  
Renin Content

1. We have examined the response of renin to chronic low and high sodium chloride intake in rats with transplanted phaeochromocytoma. 2. Phaeochromocytoma suppressed the usual elevated plasma renin activity observed during sodium deprivation. 3. Studies in isolated perfused kidneys indicated that sodium-deprived phaeochromocytoma rats released substantially less renin than sodium-deprived control rats despite an almost identical renal renin content in both sets of animals. In addition, low perfusion pressure (50 mmHg) failed to stimulate renin release in kidneys from these phaeochromocytoma rats. 4. Additional experiments demonstrated that chronic sodium chloride loading suppressed plasma renin activity, renin content and renin release in both phaeochromocytoma and control rats. Both sodium-loaded phaeochromocytoma and sodium-loaded control rats were unresponsive to low perfusion pressure. 5. We conclude that noradrenaline-secreting phaeochromocytoma impairs the response of plasma renin activity in the rat by inhibiting renin release. We also conclude that chronic sodium chloride loading has a similar effect, but the mechanisms remain to be determined.

Selective dietary potassium depletion and acid-base equilibrium in the rat

1985 ◽  
Vol 68 (3) ◽  
pp. 301-309 ◽  
Author(s):  
Pierre Girard ◽  
Monique Brun-Pascaud ◽  
Michel Paillard
Keyword(s):  
Sodium Chloride ◽  
Plasma Renin Activity ◽  
Metabolic Alkalosis ◽  
Sodium Phosphate ◽  
Plasma Renin ◽  
Group A ◽  
Group B ◽  
Excretion Rates ◽  
Neutral Sodium ◽  
K Depletion

1. K+ depletion of two kinds was induced in two groups of rats by selective dietary restriction for up to 5 weeks. Complete metabolic studies for H+, K+, Na+ and Cl− were carried out daily during weeks 1, 3 and 5. 2. In control rats of group A (receiving K+ with sodium chloride), plasma pH (7.47) and HCO−3(25 mmol/l), as well TA (titratable acid) —- HCO−3 and NH+4 urinary excretion rates, were stable, while balances were nil for K+ and slightly positive for Cl−. In K+-deprived rats of group A receiving sodium chloride, a progressive metabolic alkalosis developed (plasma pH reached 7.57 and HCO−3 35.8 mmol/l by 5 weeks), and TA - HCO−3 and NH+4 urinary excretion rates were not different from controls. Plasma K+ fell progressively from 4.20 to 2.20 mmol/l, with negative K+ balance. Balances for Na+ and H2O were highly positive and plasma renin activity and aldosterone decreased by week 5. Hypochloraemia developed with positive Cl− balance. 3. In control rats of group B (receiving K+ with neutral sodium phosphate), a slight metabolic alkalosis developed, and TA - HCO−3 excretion rate was increased compared with control rats of group A. Balances were slightly negative for K+ and Cl−. In K+-deprived rats of group B receiving neutral sodium phosphate, a profound metabolic alkalosis developed (plasma pH reached 7.60 and HCO−3 42.6 mmol/l by 5 weeks), and TA-HCO−3 and NH+4 excretion rates were at no time different from those of control rats of group B. Plasma K+ fell progressively from 4.25 to 2.30 mmol/l, and K+ balance was more negative than that in control rats of group B. Hypochloraemia developed with a negative Cl− balance. 4. In both K+-restricted groups, a linear negative correlation was observed between plasma HCO−3 (or pH) and plasma K+. These results suggest that metabolic alkalosis does occur in sustained selective K+-depletion in rats. Metabolic alkalosis could be generated essentially by net transfer of H+ from extracellular fluid (ECF) into cells, probably in exchange for K+ in the reverse direction. Metabolic alkalosis could be maintained by an increase in tubular reabsorption of filtered HCO−3, probably via an enhanced Na+/H+ exchange in the proximal tubule in sodium chloride-loaded rats, which may account for the ECF volume expansion with low plasma renin activity and aldosterone, and via an enhanced Cl−/HCO−3 exchange in distal nephron in sodium phosphate-loaded rats.

Demonstration of gonadotropin-induced plasma renin activity in human internal spermatic vein

1988 ◽  
Vol 117 (2) ◽  
pp. 268-272 ◽  
Author(s):  
Akihiko Okuyama ◽  
Masahiro Nakamura ◽  
Mikio Namiki ◽  
Masami Takeyama ◽  
Hideki Fujioka ◽  
...  
Keyword(s):  
Plasma Renin Activity ◽  
Leydig Cells ◽  
Plasma Renin ◽  
Serum Testosterone ◽  
Treated Group ◽  
Renin Activity ◽  
Spermatic Vein ◽  
Human Testis ◽  
Internal Spermatic Vein

Abstract. In order to investigate the secretion of renin from the Leydig cells of human testis, plasma renin activity (PRA) in left internal spermatic vein (ISV) and cubital vein (CV) was measured at the time of surgical repair of varicocele in 19 patients aged from 21 to 39 years. Ten of them were given a single im administration of hCG (10000 IU/m2) 4 days before the operation, whereas the remaining nine were not treated. Although mean PRA levels in CV in treated and non-treated groups were similar (1.25 ± 0.45 and 1.14 ± 0.38 nmol/l per h, respectively), mean PRA level of ISV in the treated group (3.52 ± 0.76 nmol/l per h) was significantly higher than that in the non-treated group (1.30 ± 0.32 nmol/l per h) (P < 0.01); serum testosterone levels in the same ISV were also much higher in the treated than in non-treated group (P < 0.001). These data show the following results; 1) under basal conditions, no release of renin from Leydig cells into testicular blood flow could be observed; 2) after treatment with hCG, the secretion of renin into the ISV seemed to be demonstrable. The present results suggest for the first time the secretion of hCG-induced renin from the human testis in vivo.

Plasma adrenocorticotrophin, cortisol and aldosterone responses to ovine corticotrophin-releasing factor and vasopressin in sheep

1986 ◽  
Vol 111 (1) ◽  
pp. 93-100 ◽  
Author(s):  
P. Pradier ◽  
M. J. Davicco ◽  
A. Safwate ◽  
C. Tournaire ◽  
M. Dalle ◽  
...  
Keyword(s):  
Plasma Renin Activity ◽  
Arginine Vasopressin ◽  
Plasma Levels ◽  
Maximum Level ◽  
Plasma Renin ◽  
Peak Level ◽  
Cortisol Secretion ◽  
Rapid Rise ◽  
Corticotrophin Releasing Factor ◽  
Cortisol Increase

Abstract. Ovine corticotrophin-releasing factor (oCRF) (1 μg/kg) and arginine vasopressin (AVP) (1 μg/kg) were injected iv in sheep, both separately and in combination. Plasma levels of immunoreactive ACTH (IRACTH), cortisol, and aldosterone were measured for 3 h after the injections. Mean levels before injections were 8 ± 4 pmol/l for ACTH, 7 ± 3 nmol/l for cortisol, and 28 ± 9 pmol/l for aldosterone. CRF caused a rapid rise in IR-ACTH and a peak level of 125 ± 52 pmol/l was obtained 15 min after injection. Highest values for cortisol and aldosterone levels were 40 ± 9 nmol/l and 64 ± 13 pmol/l, respectively, 30 min after injection. AVP also increased IR-ACTH (maximum level: 202 ± 77 pmol/l at 5 min) and aldosterone (128 ± 36 pmol/l at 15 min), whereas the cortisol increase was lower than after CRF. Simultaneous injection of CRF and AVP produced an addition of the IR-ACTH response (295 ± 82 pmol/l at 15 min), but the changes in cortisol levels were similar to those obtained after CRF alone and those in aldosterone levels resembled those induced by AVP alone. Plasma Na and K, osmolality, and plasma renin activity (PRA) were not modified by either CRF or AVP. It is suggested that the increase in aldosterone levels after CRF could be mediated by ACTH and that after AVP by an IR-ACTH peptide with less effect on cortisol secretion.

scholarly journals Latent Autonomous Cortisol Secretion From Apparently Nonfunctioning Adrenal Tumor in Nonlateralized Hyperaldosteronism

2019 ◽  
Vol 104 (10) ◽  
pp. 4382-4389 ◽  
Author(s):  
Youichi Ohno ◽  
Masakatsu Sone ◽  
Nobuya Inagaki ◽  
Yoshiyu Takeda ◽  
Isao Kurihara ◽  
...  
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Adrenal Tumors ◽  
Cortisol Secretion ◽  
Hormone Levels ◽  
Clinical Complications ◽  
Basal Cortisol ◽  
Autonomous Cortisol Secretion ◽  
Cortisol Levels

Abstract Context Adrenal tumors (ATs), even those diagnosed as nonfunctioning, may cause metabolic disorders. Some primary aldosteronism (PA) patients with ATs are diagnosed with bilateral PA based on adrenal venous sampling (AVS), and their ATs are apparently nonfunctioning. Objective To clarify the influence of apparently nonfunctioning ATs, we compared hormone levels and clinical complications between bilateral PA cases with and without ATs. Design, setting, and participants After retrospectively assessing 2814 patients with PA in the multicenter Japan PA study, bilateral PA cases on AVS were divided into cases with and without ATs by computed tomography findings. Importantly, patients with cortisol levels >1.8 µg/dL after the 1-mg dexamethasone suppression test (DST) were excluded. Clinical characteristics and biochemical data were compared between them. The correlation between AT size and hormone levels was also analyzed. Main outcome measures Analyzed were 196 bilateral PA patients with ATs and 331 those without ATs. Although basal cortisol and aldosterone levels were similar between them, cortisol levels after the 1-mg DST and the prevalences of diabetes mellitus and proteinuria were significantly higher and ACTH levels and plasma renin activity were significantly lower in cases with ATs than in those without. After adjusting for patients’ backgrounds, cortisol levels after the 1-mg DST and plasma renin activity remained significantly different between them. Moreover, cortisol levels after the 1-mg DST and ACTH levels correlated with AT size. Conclusions Apparently nonfunctioning ATs in bilateral PA cases may cause latent autonomous cortisol secretion, inducing diabetes and proteinuria.

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