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.

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.

EFFECTS OF VARIOUS PEPTIDES ON ALDOSTERONE PRODUCTION OF SODIUM DEFICIENT RATS

1968 ◽  
Vol 59 (2) ◽  
pp. 186-192 ◽  
Author(s):  
B. van der Wal ◽  
D. de Wied
Keyword(s):  
Angiotensin Ii ◽  
The Other ◽  
Adrenal Tissue ◽  
Acth Fragments ◽  
Aldosterone Production ◽  
Hypophysectomized Rats

ABSTRACT The effect of angiotensin II, vasopressin, ACTH, α- and β-MSH and several ACTH fragments was studied on the production of aldosterone in sodium-deficient intact and hypophysectomized rats and in animals pretreated with dexamethasone-pentobarbitone (D-N) or pentobarbitone-chlorpromazine (N-CPZ). As an index of the production of aldosterone in vivo the rate of aldosterone production by excised adrenal tissue in vitro was used. The effect of angiotensin II and vasopressin on aldosterone production was inhibited by previous hypophysectomy or by pretreatment with large amounts of dexamethasone while the action of ACTH was not affected by these measures. Except for α-MSH, none of the other ACTH-fragments was capable of stimulating the rate of aldosterone production in D-N rats. This was interpreted as indicating that the stimulatory effect of ACTH on aldosterone production in sodium-deficient rats is a property of the whole ACTH-molecule.

In vivo and in vitro effects of metoclopramide on aldosterone secretion in rats

1983 ◽  
Vol 102 (4) ◽  
pp. 589-593 ◽  
Author(s):  
Shusaku Nagahama ◽  
Masaki Fujimaki ◽  
Hiroko Suzuki ◽  
Hiroshi Kawabe ◽  
Ikuo Saito ◽  
...  
Keyword(s):  
Sodium Intake ◽  
Plasma Renin ◽  
Zona Glomerulosa ◽  
Plasma Aldosterone ◽  
Dopamine Antagonist ◽  
High Sodium ◽  
Aldosterone Production ◽  
In Vitro Effects

Abstract. This study was designed to investigate the effects of metoclopramide, a dopamine antagonist, on in vivo and in vitro aldosterone production in the rat. In addition, we examined the effect of various levels of sodium intake on the response of plasma aldosterone to metoclopramide. Metoclopramide (2–50 mg/kg) was given by ip injection to conscious rats. Metoclopramide induced a dose-related increase in plasma aldosterone, whereas it only increased plasma renin activity at high doses (20 and 50 mg/kg). The response of plasma aldosterone to 10 mg/kg of metoclopramide in the low-sodium group was greater than that in the high-sodium group. Metoclopramide had no effect on aldosterone production in isolated zona glomerulosa cells in vitro.

The actions of N-terminal fragments of corticotrophin on steroidogenesis in dispersed rat adrenal cells in vitro

1986 ◽  
Vol 109 (2) ◽  
pp. 275-278 ◽  
Author(s):  
G. P. Vinson ◽  
B. J. Whitehouse ◽  
A. Bateman ◽  
A. Dell ◽  
S. M. Laird
Keyword(s):  
Sodium Intake ◽  
Physiological Role ◽  
Cell Types ◽  
Structural Features ◽  
Zona Glomerulosa ◽  
Minimum Effective Concentration ◽  
Adrenal Cells ◽  
Aldosterone Production

ABSTRACT The finding that the rat adrenal zona glomerulosa cell shows specific sensitivity to stimulation by α-MSH and related peptides has been confirmed both in vivo and in vitro, raising the possibility that α-MSH may have a physiological role in the control of glomerulosa function and aldosterone secretion. To define more closely the structural features which confer the specificity of the glomerulosa response, other ACTH derived peptides have been tested for their specificity of actions on rat adrenal cells in vitro. The peptides tested were ACTH(5–24), ACTH(1–12), ACTH(1–14), ACTH(1–15), ACTH1–16) and ACTH(1–17). Their actions were compared with those of α-MSH and ACTH(1–24). All of the ACTH-derived peptides stimulated glomerulosa corticosterone production with sensitivities similar to that of α-MSH; minimum effective concentration was 10 nmol/l. Also, like α-MSH, the shorter ACTH peptides stimulated aldosterone production only relatively weakly in these cells from animals on normal sodium intake. Only ACTH(5–24), ACTH(1–16) and ACTH(1–17) stimulated fasciculata/reticularis cells at concentrations up to 1 μmol/l. The actions of all of the shorter peptides were thus unlike those of ACTH(1–24) which stimulates both cell types with approximately equal sensitivity, and which furthermore strongly stimulates aldosterone production. The data suggest that the 18–24 region of the ACTH molecule contains the signal for a fasciculata/ reticularis response, and the region 1–13 that for glomerulosa specificity. They confirm the view that, in the rat, α-MSH itself may be the specific pituitary glomerulosa-stimulating agent which much experimental work has predicted. They also indicate that synthetic ACTH(1–17) analogues should be used with caution. J. Endocr. (1986) 109, 275–278

scholarly journals EJE Prize 2013: Regulation of aldosterone secretion: from physiology to disease

2013 ◽  
Vol 168 (6) ◽  
pp. R85-R93 ◽  
Author(s):  
Felix Beuschlein
Keyword(s):  
High Throughput Sequencing ◽  
Secondary Hypertension ◽  
Small Sample ◽  
Cellular Systems ◽  
Common Disease ◽  
Aldosterone Secretion ◽  
Technical Developments ◽  
Starting Point

Arterial hypertension is a major cardiovascular risk factor that affects between 10 and 40% of the population in industrialized countries. Primary aldosteronism (PA) is the most common form of secondary hypertension with an estimated prevalence of around 10% in referral centers and 4% in a primary care setting. Despite its high prevalence until recently, the underlying genetic and molecular basis of this common disease had remained largely obscure. Over the past decade, a number of insights have been achieved that have relied onin vitrocellular systems, wild-type and genetically modifiedin vivomodels, as well as clinical studies in well-characterized patient populations. This progress has been made possible by a number of independent technical developments including that of specific hormone assays that allow measurement in small sample volumes as well as genetic techniques that enable high-throughput sequencing of a large number of samples. Furthermore, animal models have provided important insights into the physiology of aldosterone regulation that have served as a starting point for investigation of mechanisms involved in autonomous aldosterone secretion. Finally, national and international networks that have built up registries and biobanks have been instrumental in fostering translational research endeavors in PA. Therefore, it is to be expected that in the near future, further pathophysiological mechanisms that result in autonomous aldosterone secretion will be unraveled.

scholarly journals Additional evidence for a proform to tropoelastin from chick aorta

1979 ◽  
Vol 177 (2) ◽  
pp. 559-567 ◽  
Author(s):  
C S Heng-Khoo ◽  
R B Rucker ◽  
K W Buckingham
Keyword(s):  
Basic Protein ◽  
Cross Linking ◽  
Protein Subunit ◽  
Deficient Diet ◽  
Culture In Vitro ◽  
One Step

Evidence is presented for the presence of precursor to tropoelastin in chick arterial extracts. The precursor is approx. 100 000 daltons in size. It is suggested to be a precursor to tropoelastin (72 000 daltons). This protein may be observed in culture in vitro if appropriate precautions are taken to inhibit proteolysis. Once synthesized, it appears to be converted into tropoelastin within 10–20 min. The protein may also be detected in vivo. When 1-day-old cockerels were fed on a copper-deficient diet (less than 1 p.p.m. to inhibit cross-linking) containing epsilon-aminohexanoic acid (0.2%) to retard proteolysis and then injected wiht [3H]valine, extraction of arterial proteins 12h after injection resulted in detection of two major peaks of [3H]valine-labelled protein with pI values of pH 7.0 and 5.0 respectively. The protein that focused at pH 7.0 was estimated to be about 100 000 daltons in size and could be shown to be converted into a more basic protein with the properties of tropoelastin. It is speculated that the protein with pI 5.0 may be yet another extension peptide. The data appear to be in keeping with similar observations by ourselves and others that a proform of tropoelastin exists, and, in at least one step before conversion into tropoelastin, exists as a 100 000-dalton protein subunit.

Increased Renal Sensitivity to Aldosterone in the Potassium-Loaded Rat

1976 ◽  
Vol 51 (s3) ◽  
pp. 315s-317s
Author(s):  
W. R. Adam ◽  
J. W. Funder
Keyword(s):  
Sodium Intake ◽  
Control Diet ◽  
High Potassium ◽  
High Sodium ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
High K ◽  
And Control

1. The renal response to aldosterone (urinary sodium and potassium excretion) was determined in adrenalectomized rats previously fed either a high potassium diet or a control diet. High K+ rats showed an enhanced response to aldosterone at all doses tested. 2. This enhanced response to aldosterone required the presence of the adrenal glands during the induction period, could be suppressed by a high sodium intake, but could not be induced by a low sodium diet. 3. No difference between high K+ and control rats could be detected in renal mineralocorticoid receptors, assessed by both in vivo and in vitro binding of tritiated aldosterone. 4. The method of the induction, and the mechanism of the enhanced response, remain to be defined.

Correlation between magnesium and potassium contents in muscle: role of Na(+)-K+ pump

1993 ◽  
Vol 264 (2) ◽  
pp. C457-C463 ◽  
Author(s):  
I. Dorup ◽  
T. Clausen
Keyword(s):  
Extensor Digitorum Longus ◽  
Extensor Digitorum ◽  
Deficient Diet ◽  
Young Rats ◽  
Wide Range ◽  
86Rb Influx

In young rats fed a Mg(2+)-deficient diet for 3 wk, Mg2+ and K+ contents in soleus and extensor digitorum longus muscles were significantly reduced and closely correlated. In isolated soleus muscles, Mg2+ depletion induced an even more pronounced loss of K+, and Mg2+ and K+ contents were correlated over a wide range (r = 0.95, P < 0.001). Extracellular Mg2+ (0-1.2 mM) caused no change in total or ouabain-suppressible 86Rb influx. After long-term incubation in Ca(2+)-Mg(2+)-free buffer with EDTA and EGTA, cellular Mg2+ and K+ contents were reduced by 35 and 15%, respectively, without any reduction in ATP and total or ouabain-suppressible 86Rb influx. In Mg(2+)-depleted muscles 42K efflux was increased by up to 42%, and repletion with Mg2+ produced a graded decrease. We conclude that Mg2+ and K+ contents are closely correlated in muscles Mg2+ depleted in vivo or in vitro and that neither extracellular nor moderate intracellular Mg2+ depletion affects total or Na(+)-K+ pump-mediated K+ influx. The reduced K+ content may rather be related to increased K+ efflux from the muscles.

scholarly journals Collecting Duct Is a Site of Sodium Retention in PAN Nephrosis: A Rationale for Amiloride Therapy

2001 ◽  
Vol 12 (3) ◽  
pp. 598-601 ◽  
Author(s):  
GEORGES DESCHÊNES ◽  
MONIKA WITTNER ◽  
ANTONIO DI STEFANO ◽  
SYLVIE JOUNIER ◽  
ALAIN DOUCET
Keyword(s):  
Collecting Duct ◽  
Urinary Sodium Excretion ◽  
Sodium Balance ◽  
Sodium Reabsorption ◽  
Puromycin Aminonucleoside ◽  
Aldosterone Receptor ◽  
Collecting Tubules ◽  
A Site

Abstract. Micropuncture studies of the distal nephron and measurements of Na,K-ATPase activity in microdissected collecting tubules have suggested that renal retention of sodium in puromycin aminonucleoside (PAN) nephrotic rats originates in the collecting duct. The present study demonstrated this hypothesis by in vitro microperfusion and showed that amiloride was able to restore sodium balance. Indeed, isolated perfused cortical collecting ducts from PAN-treated rats exhibited an abnormally high transepithelial sodium reabsorption that was abolished by amiloride, and in vivo administration of amiloride fully prevented decreased urinary sodium excretion and positive sodium balance in nephrotic rats. As expected from the aldosterone independence of Na+ retention in PAN nephrotic rats, blockade of aldosterone receptor by potassium canrenoate did not alter urinary Na+ excretion, Na+ balance, or ascites formation in PAN nephrotic rats.

scholarly journals Role of pyridoxal phosphate in mammalian polyamine biosynthesis. Lack of requirement for mammalian S-adenosylmethionine decarboxylase activity

1977 ◽  
Vol 166 (1) ◽  
pp. 81-88 ◽  
Author(s):  
A E Pegg
Keyword(s):  
Ornithine Decarboxylase ◽  
Pyridoxal Phosphate ◽  
Vitamin B ◽  
Decarboxylase Activity ◽  
Deficient Diet ◽  
Polyamine Biosynthesis ◽  
Adenosylmethionine Decarboxylase ◽  
Ornithine Decarboxylase Activity

1. Polyamine concentrations were decreased in rats fed on a diet deficient in vitamin B-6. 2. Ornithine decarboxylase activity was decreased by vitamin B-6 deficiency when assayed in tissue extracts without addition of pyridoxal phosphate, but was greater than in control extracts when pyridoxal phosphate was present in saturating amounts. 3. In contrast, the activity of S-adenosylmethionine decarboxylase was not enhanced by pyridoxal phosphate addition even when dialysed extracts were prepared from tissues of young rats suckled by mothers fed on the vitamin B-6-deficient diet. 4. S-Adenosylmethionine decarboxylase activities were increased by administration of methylglyoxal bis(guanylhydrazone) (1,1′-[(methylethanediylidine)dinitrilo]diguanidine) to similar extents in both control and vitamin B-6-deficient animals. 5. The spectrum of highly purified liver S-adenosylmethionine decarboxylase did not indicate the presence of pyridoxal phosphate. After inactivation of the enzyme by reaction with NaB3H4, radioactivity was incorporated into the enzyme, but was not present as a reduced derivative of pyridoxal phosphate. 6. It is concluded that the decreased concentrations of polyamines in rats fed on a diet containing vitamin B-6 may be due to decreased activity or ornithine decarboxylase or may be caused by an unknown mechanism responding to growth retardation produced by the vitamin deficiency. In either case, measurements of S-adenosylmethionine decarboxylase and ornithine decarboxylase activity under optimum conditions in vitro do not correlate with the polyamine concentrations in vivo.

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