THE ROLE OF A FEEDBACK MECHANISM IN THE REGULATION OF ALDOSTERONE SECRETION IN THE RAT

1973 ◽  
Vol 73 (2) ◽  
pp. 282-288
Author(s):  
L. Debreceni ◽  
B. Csete
Keyword(s):  
Marked Decrease ◽  
Feedback Regulation ◽  
Feedback Mechanism ◽  
The Other ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Aldosterone Secretion ◽  
Aldosterone Production

ABSTRACT The effect of prolonged aldosterone and DOC treatment in the in vitro aldosterone production was studied in the rat. When the animals were supplied with food containing 16.5 mEq./100 g of sodium, both aldosterone and DOC treatment led to a marked decrease in aldosterone production. On the other hand, under dietary sodium restriction both aldosterone and DOC treatment failed to induce a suppression of the elevated aldosterone production. On the basis of these findings, it seems that a sufficient sodium supply of the organism is necessary for the control of aldosterone secretion either by an increase of aldosterone production or DOC treatment if any feedback regulation is involved in the mechanism controlling aldosterone secretion.

scholarly journals Prolactin and Male Fertility: The Long and Short Feedback Regulation

2009 ◽  
Vol 2009 ◽  
pp. 1-13 ◽  
Author(s):  
M. K. Gill-Sharma
Keyword(s):  
Chromatin Condensation ◽  
Feedback Regulation ◽  
Pituitary Hormones ◽  
Feedback Mechanism ◽  
Reproductive Hormones ◽  
Male Rats ◽  
Normal Men

In the last 20 years, a pituitary-hypothalamus tissue culture system with intact neural and portal connections has been developed in our lab and used to understand the feedback mechanisms that regulate the secretions of adenohypophyseal hormones and fertility of male rats. In the last decade, several in vivo rat models have also been developed in our lab with a view to substantiate the in vitro findings, in order to delineate the role of pituitary hormones in the regulation of fertility of male rats. These studies have relied on both surgical and pharmacological interventions to modulate the secretions of gonadotropins and testosterone. The interrelationship between the circadian release of reproductive hormones has also been ascertained in normal men. Our studies suggest that testosterone regulates the secretion of prolactin through a long feedback mechanism, which appears to have been conserved from rats to humans. These studies have filled in a major lacuna pertaining to the role of prolactin in male reproductive physiology by demonstrating the interdependence between testosterone and prolactin. Systemic levels of prolactin play a deterministic role in the mechanism of chromatin condensation during spermiogenesis.

INFLUENCE OF THE ANTERIOR PITUITARY ON THE ALDOSTERONE SECRETORY RESPONSE TO DIETARY SODIUM RESTRICTION IN THE RAT

1968 ◽  
Vol 42 (3) ◽  
pp. 465-475 ◽  
Author(s):  
T. C. LEE ◽  
B. van der WAL ◽  
D. de WIED
Keyword(s):  
Anterior Pituitary ◽  
Normal Diet ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Aldosterone Production ◽  
Hypophysectomized Rats ◽  
Dietary Sodium Restriction ◽  
Long Acting ◽  
Intact Rats

SUMMARY Studies of the rate of aldosterone production in vitro of adrenals of rats hypophysectomized before dietary sodium restriction showed that hypophysectomy not only prevented the increases in aldosterone production observed in intact, Na-deprived rats, but also depressed the level of aldosterone production to below that of intact rats maintained on a normal diet. Rats hypophysectomized for a similar period of time but maintained on the normal diet showed a similar decrease. Experiments on adeno- and neuro-hypophysectomized rats indicated that the pituitary factor required for the normal mineralocorticoid response to dietary sodium restriction resides in the anterior pituitary. Treatment of hypophysectomized rats during dietary sodium restriction with doses of a long-acting corticotrophin (ACTH) prevented adrenal atrophy and maintained a normal glucocorticoid response to intravenous injections of ACTH, but failed to increase aldosterone production rates in vitro to levels above that of intact rats on a normal diet; it also failed to restore the enhanced adrenocortical sensitivity to the stimulating effect of aldosterone production of intravenously injected ACTH which is characteristic of acutely hypophysectomized, Na-deficient rats. Treatment with anterior pituitary powder (8–12 mg./day) for similar periods, however, restored the aldosterone production of adrenals in vitro of hypophysectomized, Na-deprived rats to levels nearly indistinguishable from those of acutely hypophysectomized, Na-deprived controls. The same doses of anterior pituitary powder were shown not to have any demonstrable effect on the aldosterone production of adrenals in vitro of intact rats on a normal diet. These results are interpreted as indicating the existence of a pituitary factor other than ACTH which stimulates aldosterone secretion. This factor does not appear to act directly on the adrenal cortex or to stimulate the secretion of specific glomerulotropic substances, but probably exerts its effect by maintaining the normal functional capacity of some as yet undefined tissues which secrete glomerulotropic substances in response to dietary sodium restriction.

THE REGULATION OF ALDOSTERONE PRODUCTION IN NORMAL AND SODIUM-DEFICIENT RATS

1968 ◽  
Vol 41 (2) ◽  
pp. 179-188 ◽  
Author(s):  
M. F. D. CSÁNKY ◽  
B. van der WAL ◽  
D. de WIED
Keyword(s):  
Dietary Sodium ◽  
Sodium Balance ◽  
Standard Diet ◽  
Aldosterone Secretion ◽  
Deficient Diet ◽  
Enhanced Production ◽  
Aldosterone Production ◽  
High Doses ◽  
Long Acting

SUMMARY Aldosterone secretion of rats on a standard diet, as determined by the rate of aldosterone produced by adrenal tissue in vitro, was not affected by exposure to ether, by hypophysectomy or by nephrectomy. Administration of high doses of long-acting corticotrophin (ACTH; 1·5 units) to rats hypophysectomized 24 hr. previously also failed to affect the rate of aldosterone production in vitro in rats on the standard diet. Only hypophysectomy and nephrectomy in the same rat induced a significant decrease in aldosterone production in vitro 6 hr. after operation in rats fed the standard diet. Aldosterone production in vitro increased in rats fed a sodium-deficient diet. The increment was more pronounced in rats maintained on the diet for 14- than for 10-days. Hypophysectomy, or nephrectomy, caused no decrease in aldosterone production, when compared to sham-operated rats. However, hypophysectomy and nephrectomy together caused a marked decline in the rate of aldosterone production in vitro 6 hr. after operation as compared with sham-operated or non-operated rats. The administration of relatively small amounts of ACTH (8 m-u.) induced a marked increase in the rate of aldosterone production in vitro of intact, and hypophysectomized sodium-deficient rats. The results indicate that in the rat, as in other species, both the kidney and the pituitary contribute to the maintenance of the basal rate of aldosterone production in animals in normal sodium-balance and that these organs are responsible for the increased rate of aldosterone production in dietary sodium restriction. ACTH, however, though a potent stimulus for aldosterone secretion, appears only to augment the already enhanced production of aldosterone in the sodium-deprived rat.

EFFECT OF GROWTH HORMONE ON THE ALDOSTERONE SECRETORY RESPONSE TO SODIUM RESTRICTION IN CORTICOTROPHIN-MAINTAINED HYPOPHYSECTOMIZED NEPHRECTOMIZED RATS

1971 ◽  
Vol 51 (2) ◽  
pp. 369-374 ◽  
Author(s):  
M. PALKOVITS ◽  
J. J. T. W. A. STRIK ◽  
W. de JONG ◽  
D. de WIED
Keyword(s):  
Growth Hormone ◽  
Plasma Potassium ◽  
Secretory Response ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Sodium Deficiency ◽  
Aldosterone Production ◽  
Hypophysectomized Rats ◽  
Previously Treated

SUMMARY The rate of aldosterone production in vitro by adrenal glands from rats hypophysectomized 7 days previously, treated with corticotrophin (ACTH) and subjected to dietary sodium restriction for 2 weeks, was decreased 6 h after nephrectomy. However, 18 h and 48 h after nephrectomy there was a marked increase in the rate of aldosterone production in vitro. In addition there was a rise in the plasma potassium concentration. These results indicated that in order to detect whether the influence of growth hormone on aldosterone secretory response to sodium restriction in hypophysectomized rats was mediated by the kidney, studies had to be performed within 6 h after removal of the kidneys. Since the effect of growth hormone on aldosterone production requires 2 days to develop (Palkovits, de Jong, van der Wal & de Wied, 1971), rats hypophysectomized 54 h previously were used. The kidneys were removed 6 h before decapitation. In these animals, the administration of growth hormone in the presence of ACTH restored the aldosterone secretory response to sodium deficiency. The results suggest that growth hormone maintains the aldosterone secretory response to sodium restriction in hypophysectomized rats in the absence of the kidneys.

EFFECT OF PROSTAGLANDIN E2 AND A2 ON STEROID SYNTHESIS BY THE RAT ADRENAL GLAND

1975 ◽  
Vol 65 (1) ◽  
pp. 55-63 ◽  
Author(s):  
A. SPÄT ◽  
SARA JÓZAN
Keyword(s):  
Adrenal Gland ◽  
Prostaglandin E2 ◽  
Adrenal Glands ◽  
Prostaglandin E ◽  
Sodium Restriction ◽  
Aldosterone Secretion ◽  
Steroid Synthesis ◽  
Aldosterone Production ◽  
Hypophysectomized Rats

SUMMARY Prostaglandin E2 increased aldosterone output by superfused capsular adrenal glands obtained from sodium-repleted, hypophysectomized rats but corticosterone did not show a statistically significant increase. Prostaglandin A2 increased corticosterone but not aldosterone production by incubated capsular glands obtained from sodium-repleted, hypophysectomized rats. Both aldosterone and corticosterone production rates were increased by PGA2 after previous sodium restriction. Corticosterone production rate of the decapsulated adrenal gland was not significantly modified by prostaglandin A2 in a concentration effective on the capsular adrenal gland. A possible role of prostaglandins in the regulation of aldosterone secretion is discussed.

ALDOSTERONE STIMULATION IN VITRO

1965 ◽  
Vol 50 (2) ◽  
pp. 301-309 ◽  
Author(s):  
Jürg Müller
Keyword(s):  
Ammonium Chloride ◽  
Human Urine ◽  
Incubation Medium ◽  
The Other ◽  
Ammonium Ions ◽  
Response Curves ◽  
Urine Extract ◽  
Similar Dose ◽  
Aldosterone Production

ABSTRACT An extract of human urine, which was previously shown to stimulate aldosterone production by rat adrenal sections, was further purified. Evidence was obtained that its aldosterone-stimulating effect was due to the presence of ammonium ions. Addition of ammonium chloride and of urine extract to the incubation medium caused identical increases in aldosterone production in vitro. In addition to ammonium ions, rubidium and caesium ions also stimulated aldosterone production up to 250% that of control values without a significant effect on corticosterone production. Similar dose-response curves were obtained when increasing concentrations of potassium, ammonium, rubidium and caesium ions were tested. Aldosterone production was maximal at concentrations of 7 mval/1 and was significantly lower at higher concentrations. When ammonium chloride and ACTH were simultaneously added to the incubation medium, the production of aldosterone and of corticosterone was lower than with ACTH alone. On the other hand, the stimulating activity on aldosterone and corticosterone production by »TPN« (NADP) and glucose-6-phosphate was enhanced by the simultaneous addition of ammonium chloride.

Dissociation in plasma renin and adrenal ANG II and aldosterone responses to sodium restriction in rats

1991 ◽  
Vol 261 (4) ◽  
pp. E487-E494 ◽  
Author(s):  
A. Menachery ◽  
L. M. Braley ◽  
I. Kifor ◽  
R. Gleason ◽  
G. H. Williams
Keyword(s):  
Plasma Renin ◽  
Fold Increase ◽  
Plasma Aldosterone ◽  
Delayed Response ◽  
Ang Ii ◽  
Sodium Restriction ◽  
Sodium Depletion ◽  
Pathway Activity

In rats, plasma renin activity (PRA) increases sharply, reaching a plateau within hours of sodium restriction. Plasma aldosterone increases gradually, not reaching a plateau for 1-2 days. To determine whether this dissociation is secondary to the time needed to modify adrenal sensitivity to angiotensin II (ANG II) and to assess the role of locally produced ANG II in this process, rats were salt restricted for 0-120 h. Plasma hormone levels were assessed, adrenal ANG II was measured, and basal and ANG II (1 x 10(-8) M)-stimulated steroidogenesis were determined in vitro. Although PRA attained an elevated plateau within 8 h, plasma aldosterone did not peak until after 48 h of sodium depletion. The in vitro aldosterone sensitivity to exogenous ANG II was not apparent until rats had been salt restricted for 16 h. A plateau (4-fold increase above the ANG II response on high salt) was achieved between 24 and 48 h. Adrenal ANG II also exhibited a similar delayed response that correlates significantly with changes in aldosterone biosynthesis and late pathway activity. Thus the dissociation between PRA and plasma aldosterone may be secondary to a lag in the zona glomerulosa's (ZG) steroidogenic response to ANG II as well as a parallel lag in tissue ANG II production, suggesting that changes in tissue ANG II may mediate ZG sensitivity to ANG II during sodium deprivation.

scholarly journals Impact of GPR1 signaling on maternal high-fat feeding and placenta metabolism in mice

2019 ◽  
Vol 316 (6) ◽  
pp. E987-E997 ◽  
Author(s):  
Binbin Huang ◽  
Chen Huang ◽  
Huashan Zhao ◽  
Wen Zhu ◽  
Baobei Wang ◽  
...  
Keyword(s):  
Biological Effects ◽  
Negative Control ◽  
Feedback Mechanism ◽  
High Fat ◽  
Fatty Acid Binding ◽  
Maternal Metabolism ◽  
Phosphorylated Akt

Chemerin and G protein-coupled receptor 1 (GPR1) are increased in serum and placenta in mice during pregnancy. Interestingly, we observed increased serum chemerin levels and decreased GPR1 expression in placenta of high-fat-diet-fed mice compared with chow-fed mice at gestational day 18. GPR1 protein and gene levels were significantly decreased in gestational diabetes mellitus (GDM) patient placentas. Therefore, we hypothesized that chemerin/GPR1 signaling might participate in the pathogenic mechanism of GDM. We investigated the role of GPR1 in carbohydrate homeostasis during pregnancy using pregnant mice transfected with small interfering RNA for GPR1 or a negative control. GPR1 knockdown exacerbated glucose intolerance, disrupted lipid metabolism, and decreased β-cell proliferation and insulin levels. Glucose transport protein-3 and fatty acid binding protein-4 were downregulated with reducing GPR1 in vivo and in vitro via phosphorylated AKT pathway. Taken together, our findings first demonstrate the expression of GPR1, the characterization of its direct biological effects in humans and mice, as well as the molecular mechanism that indicates the role of GPR1 signaling in maternal metabolism during pregnancy, suggesting a novel feedback mechanism to regulate glucose balance during pregnancy, and GPR1 could be a potential target for the detection and therapy of GDM.

DECREASED ALDOSTERONE PRODUCTION BY RAT ADRENAL TISSUE IN VITRO DUE TO TREATMENT WITH 9α-FLUOROCORTISOL, DEXAMETHASONE AND ADRENOCORTICOTROPHIN IN VIVO

1970 ◽  
Vol 63 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Jürg Müller
Keyword(s):  
Sodium Intake ◽  
Sodium Balance ◽  
Potassium Ions ◽  
Aldosterone Secretion ◽  
Deficient Diet ◽  
Adrenal Tissue ◽  
Aldosterone Production ◽  
Unknown Control

ABSTRACT Quartered adrenal glands of rats treated with 9α-fluorocortisol, dexamethasone or adrenocorticotrophin (ACTH) for two weeks were found to produce 70–90% less aldosterone in vitro than the adrenal tissue of untreated animals. The same fractional decreases in aldosterone production were observed when the adrenal tissue was incubated under basal conditions or was stimulated by serotonin, potassium ions or ACTH. In rats kept on a sodium-deficient diet, treatment with dexamethasone and ACTH, respectively, impaired aldosterone production to the same extent as in rats on a normal sodium intake, whereas treatment with 9α-fluorocortisol was almost completely ineffective. These results indicate that inhibition of aldosterone secretion by an exogenous mineralocorticosteroid is mediated by changes in sodium balance. On the other hand, high levels of exogenous or endogenous glucocorticosteroids apparently decrease aldosterone production by a yet unknown control mechanism which is independent of sodium intake.

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