FURTHER STUDIES ON THE SECRETION OF ALDOSTERONE BY THE RAT ADRENAL GLAND

1959 ◽  
Vol 19 (4) ◽  
pp. 310-324 ◽  
Author(s):  
BERTHA SINGER
Keyword(s):  
Skeletal Muscle ◽  
Drinking Water ◽  
Metabolic Alkalosis ◽  
Intraperitoneal Administration ◽  
Electrolyte Composition ◽  
Adrenal Vein ◽  
Aldosterone Secretion ◽  
Dietary Potassium ◽  
Low Salt ◽  
Aldosterone Production

SUMMARY 1. In rats fed normal diets, the intravenous, subcutaneous or intraperitoneal administration of potassium chloride, either immediately or at graded intervals before the collection of adrenal vein blood, did not increase the secretion of aldosterone. In animals fed low salt diets, excess of dietary potassium did not result in an increase in the secretion of aldosterone. 2. Chloride deficiency in the diet, for a period of 2 weeks, did not affect the rate of aldosterone production. 3. The intravenous administration of hypertonic saline just prior to collection of adrenal vein blood did not affect the rate of aldosterone secretion, but substitution of saline for drinking water for a period of 1 week reduced it. 4. Production of metabolic acidosis resulted in increased secretion of aldosterone. Production of metabolic alkalosis did not affect it. It is concluded from these results that altering the intracellular electrolyte composition of skeletal muscle will not affect the secretion of aldosterone. 5. Removal of peripheral blood either 2 hr, or 26 + 2 hr, before collection of adrenal vein blood in animals fed normal or low salt diets did not influence the secretion of aldosterone. Neither did maintaining the blood volume, with freshly drawn rat blood, during the collection of adrenal vein blood. 6. It was not possible to prevent the release of ACTH associated with the collection of adrenal vein blood by the use of morphine.

Properties of 5′-deiodinase of 3,3′,5′-triiodothyronine in rat skeletal muscle

1989 ◽  
Vol 120 (1) ◽  
pp. 69-74 ◽  
Author(s):  
Fujiko Tsukahara ◽  
Teruko Nomoto ◽  
Michiko Maeda
Keyword(s):  
Skeletal Muscle ◽  
Drinking Water ◽  
Incubation Medium ◽  
Marked Reduction ◽  
Daily Administration ◽  
Type I ◽  
Rat Skeletal Muscle ◽  
Thyroid Status ◽  
Altered Thyroid

Abstract. To characterize rT3 5′-deiodinase (5′D) in rat skeletal muscle, the effects of altered thyroid status and PTU on rT3 5′D were studied. rT3 5′D activity was measured by incubating homogenates of rat skeletal muscle with [125]rT3, iodine labelled in the outer ring, in the presence of 20 mmol/l DL-dithiothreitol. This activity was observed to increase significantly 24 h after a single sc injection of T3 (75 μg/kg). The increase following the daily administration of this drug (15 or 75 μg/kg) for 3 and 14 days was dependent on the dose and number of previous days of injection. A significant decrease in activity was observed 2 weeks after thyroidectomy. The addition of 0.1 mmol/l 6-n-propyl-2-thiouracil (PTU) to the incubation medium in vitro caused a marked reduction in the activity in homogenates of skeletal muscle from hypothyroid, euthyroid and hyperthyroid rats. PTU, present at 0.05% in the drinking water for 2 weeks virtually abolished it. The properties of rT3 5′D in rat skeletal muscle thus appear to be essentially the same as those of type I enzyme with respect to response toward altered thyroid status and PTU.

scholarly journals The place of ARBs in heart failure therapy: is aldosterone suppression the key?

2019 ◽  
Vol 13 ◽  
pp. 175394471986813 ◽  
Author(s):  
Uma Markan ◽  
Samhitha Pasupuleti ◽  
Celina M. Pollard ◽  
Arianna Perez ◽  
Beatrix Aukszi ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Short Review ◽  
The United States ◽  
Aldosterone Secretion ◽  
Drug Classes ◽  
Aldosterone Production ◽  
United States Food ◽  
States Food ◽  
Molecular Effects

Since the launch of the first orally available angiotensin II (AngII) type 1 receptor (AT1R) blocker (ARB) losartan (Cozaar) in the late 1990s, the class of ARBs (or ‘sartans’, short for Angiotensin-RecepTor-ANtagonistS) quickly expanded to include candesartan, eprosartan, irbesartan, valsartan, telmisartan, and olmesartan. All ARBs have high affinity for the AT1 receptor, expressed in various tissues, including smooth muscle cells, heart, kidney, and brain. Since activation of AT1R, the target of these drugs, leads, among other effects, to vascular smooth muscle cell growth, proliferation and contraction, activation of fibroblasts, cardiac hypertrophy, aldosterone secretion from the adrenal cortex, thirst-fluid intake (hypervolemia), etc., the ARBs are nowadays one of the most useful cardiovascular drug classes used in clinical practice. However, significant differences in their pharmacological and clinical properties exist that may favor use of particular agents over others within the class, and, in fact, two of these drugs, candesartan and valsartan, continuously appear to distinguish themselves from the rest of the ‘pack’ in recent clinical trials. The reason(s) for the potential superiority of these two agents within the ARB class are currently unclear but under intense investigation. The present short review gives an overview of the clinical properties of the ARBs currently approved by the United States Food and Drug Administration, with a particular focus on candesartan and valsartan and the areas where these two drugs seem to have a therapeutic edge. In the second part of our review, we outline recent data from our laboratory (mainly) on the molecular effects of the ARB drugs on aldosterone production and on circulating aldosterone levels, which may underlie (at least in part) the apparent clinical superiority of candesartan (and valsartan) over most other ARBs currently in clinical use.

Abstract 132: Leptin-mediated Aldosterone Secretion Causes Hypertension in Obese Females

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Eric J Belin de Chantemèle ◽  
Miriam Cortez-Cooper ◽  
Joseph Cannon ◽  
Anne-Cécile Huby
Keyword(s):  
Leptin Receptor ◽  
Tyrosine Phosphatase ◽  
Plasma Aldosterone ◽  
Adult Women ◽  
Aldosterone Secretion ◽  
Plasma Angiotensin ◽  
Aldosterone Production ◽  
Β Adrenergic Receptors ◽  
Dose Dependent Increase ◽  
Dose Dependent

Obesity causes hypertension (HTN) in males and females. While leptin contributes to obesity-induced HTN by increasing sympathetic activity, in males, it is unknown whether similar mechanisms trigger HTN in obese females. Females secrete 3 to 4 times more leptin than males, but do not exhibit high sympathetic tone with obesity. They however show inappropriately high aldosterone levels that positively correlate with adiposity and blood pressure (BP). Here we hypothesized that leptin induces HTN by increasing aldosterone production in obese females. Hypersensitivity to leptin, in lean mice deficient in protein tyrosine phosphatase 1B (PTP1B) or high leptin levels, in obese Agouti (Ay/a) mice induced HTN (WT: 115±2; KO: 124±2; a/a: 113±1; Ay/a: 128±7mmHg, p<0.05) but did not increase sympathetic control of BP (response to ganglionic blockade). Leptin sensitization and obesity however elevated plasma aldosterone levels and adrenal aldosterone synthase (CYP11B2) expression, in females. Chronic leptin (KO+AA: 115±5; Ay/a+AA: 114±5mmHg) or mineralocorticoid (KO+spiro:111±5; Ay/a+spiro: 121±6mmHg) receptors inhibition restored BP to baseline levels in females PTP1B KO and obese agouti mice. Leptin or leptin receptor deficiency in female ob/ob and db/db mice, abolished obesity-induced increases in adrenal CYP11B2 and plasma aldosterone while chronic leptin infusion in female mice triggered a dose-dependent increase in adrenal CYP11B2 and plasma aldosterone levels. Leptin-mediated aldosterone secretion was independent of changes in plasma angiotensin II, potassium and corticosterone (index of ACTH levels) and preserved in the presence of losartan or α and β-adrenergic receptors antagonists. Stimulation of human adrenocortical cells with leptin dose-dependently increased CYP11B2 expression and aldosterone production. While investigating the interaction between percentage of body fat, leptin and aldosterone levels in young healthy adult Caucasians we reported a positive correlation between adiposity and aldosterone, and between leptin and aldosterone in adult women only. Together these data suggest that leptin directly regulates aldosterone secretion and that leptin induces HTN via aldosterone dependent mechanisms in obese females.

scholarly journals Glikogen Otot Rangka Ayam Broiler (Gallus gallus) setelah Pemberian Teh Kombucha dalam Air Minum

2019 ◽  
Vol 20 (2) ◽  
pp. 78
Author(s):  
Nasrul Fathoni ◽  
M Anwar Djaelani ◽  
Sri Isdadiyanto
Keyword(s):  
Skeletal Muscle ◽  
Drinking Water ◽  
Body Weight ◽  
Green Tea ◽  
Muscle Glycogen ◽  
Broiler Chickens ◽  
Gallus Gallus ◽  
Feed Consumption ◽  
Skeletal Muscle Glycogen ◽  
Kombucha Tea

Kombucha tea beverage obtained by fermenting sweetened green tea for 12 days with Acetobacter xylinum and Saccharomyces which produce various kinds of organic acids, vitamins, and acts as a probiotic. The role of kombucha tea as a growth promoter is to that improve the metabolic process in the digestion of broiler chickens, so that nutrients can and fulfilled optimally for growth and development. The aim of this research was to analyze the sceletal muscle glycogen glycogen (Gallus gallus) after treat with kombucha tea in drinking water. Kombucha tea used is the result of fermentation of green tea for 12 days. This research used DOC chickens (Day Old Chicken) as much as 20 randomly divided into 4 treatments with concentration ie 0%, 10%, 20%, and 40% kombucha tea in drinking water for 32 days. The variables measured were skeletal muscle glycogen levels, body weight, feed consumption and drink consumption. The data obtained were analyzed using ANOVA followed by Duncan Test with 95% confidence level using SPSS 17.0 software. The results of this study showed that kombucha tea on skeletal muscle glycogen and feed consumption showed no significant difference, while on body weight and drink consumption showed significantly different results. Based on the results of the study, it can be concluded that giving kombucha tea in drinking water to a concentration of 40% has not been able to affect the skeletal muscle glycogen in broiler chickens. Key words: Kombucha tea, broiler chicken, glycogen skeletal muscle

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.

scholarly journals Aldosterone secretion in patients with septic shock: a prospective study

2013 ◽  
Vol 57 (8) ◽  
pp. 636-641 ◽  
Author(s):  
Rafael Barberena Moraes ◽  
Gilberto Friedman ◽  
Marina Verçoza Viana ◽  
Tiago Tonietto ◽  
Henrique Saltz ◽  
...  
Keyword(s):  
Septic Shock ◽  
Serum Levels ◽  
Zona Glomerulosa ◽  
High Dose ◽  
Zona Fasciculata ◽  
Cortisol Secretion ◽  
Aldosterone Secretion ◽  
Acth Stimulation ◽  
Aldosterone Production ◽  
A Prospective Study

OBJECTIVE: To assess serum levels of the main factors that regulate the activation of the zona glomerulosa and aldosterone production in patients with septic shock, as well as their response to a high-dose (250 µg) adrenocorticotropic hormone (ACTH) stimulation test. SUBJECTS AND METHODS: In 27 patients with septic shock, baseline levels of aldosterone, cortisol, ACTH, renin, sodium, potassium, and lactate were measured, followed by a cortrosyn test. RESULTS: Renin correlated with baseline aldosterone and its variation after cortrosyn stimulation. Baseline cortisol and its variation did not correlate with ACTH. Only three patients had concomitant dysfunction of aldosterone and cortisol secretion. CONCLUSIONS: Activation of the zona glomerulosa and zona fasciculata are independent. Aldosterone secretion is dependent on the integrity of the renin-angiotensin-aldosterone system, whereas cortisol secretion does not appear to depend predominantly on the hypothalamic-pituitary-adrenal axis. These results suggest that activation of the adrenal gland in critically ill patients occurs by multiple mechanisms.

Cytokines and endotoxin induce cytokine receptors in skeletal muscle

2000 ◽  
Vol 279 (1) ◽  
pp. E196-E205 ◽  
Author(s):  
Yan Zhang ◽  
Geneviève Pilon ◽  
André Marette ◽  
Vickie E. Baracos
Keyword(s):  
Skeletal Muscle ◽  
Interleukin 1 ◽  
Intraperitoneal Administration ◽  
Interferon Γ ◽  
Receptor Expression ◽  
Cytokine Receptor ◽  
Cytokine Receptors ◽  
Type I ◽  
Skeletal Muscle Function ◽  
Tnf Α

Proinflammatory cytokines are important factors in the regulation of diverse aspects of skeletal muscle function; however, the muscle cytokine receptors mediating these functions are uncharacterized. Binding kinetics (dissociation constant = 39 ± 4.7 × 10−9M, maximal binding = 3.5 ± 0.23 × 10−12mol/mg membrane protein) of muscle tumor necrosis factor (TNF) receptors were obtained. Skeletal muscle was found to express mRNAs encoding interleukin-1 type I and II receptors, interleukin-6 receptor (IL-6R), and interferon-γ receptor by RT-PCR, but these receptors were below limits of detection of ligand-binding assay (≥1 fmol binding sites/mg protein). Twenty-four hours after intraperitoneal administration of endotoxin to rats, TNF receptor type II (TNFRII) and IL-6R mRNA were increased in skeletal muscle ( P < 0.05). In cultured L6 cells, the expression of mRNA encoding TNFRII and IL-6R receptors was induced by TNF-α, and all six cytokine receptor mRNA were induced by a mixture of TNF-α, IFN-γ, and endotoxin ( P < 0.05). This suggests that the low level of cytokine receptor expression is complemented by a capacity for receptor induction, providing a clear mechanism for amplification of cytokine responses at the muscle level.

A Role for β-Melanotropin in the Regulation of Aldosterone Secretion during Sodium Deficiency in the Rat

1982 ◽  
Vol 63 (s8) ◽  
pp. 93s-95s ◽  
Author(s):  
Minoru Yamakado ◽  
Roberto Franco-Saenz ◽  
Patrick J. Mulrow
Keyword(s):  
Sodium Depletion ◽  
Aldosterone Secretion ◽  
Sodium Deficiency ◽  
Aldosterone Level ◽  
Adrenal Cells ◽  
Melanocyte Stimulating Hormone ◽  
Significant Stimulation ◽  
Late Step ◽  
Aldosterone Production ◽  
Corticosterone Response

1. The effect of sodium deficiency on adrenal sensitivity to β-melanotropin (β-melanocyte stimulating hormone; β-MSH) and the effect of β-MSH on a late step of aldosterone biosynthesis were studied using collagenase-dispersed rat adrenal cells. 2. Sodium depletion enhanced the sensitivity of the adrenal glomerulosa cells to β-MSH, resulting in a shift of the dose-response curve to the left, so that doses of β-MSH within the physiological range caused significant stimulation of aldosterone production. 3. The aldosterone level obtained by maximum doses of β-MSH was similar to that obtained after angiotensin (‘angiotensin II’; ANGII) during sodium depletion. 4. Sodium depletion did not change the corticosterone response to β-MSH by decapsular cells. 5. Similarly to ANGII, β-MSH significantly stimulated the conversion of exogenous corticosterone into aldosterone in the presence of an inhibitor of 3β-hydroxysteroid dehydrogenase, WIN 19,578. 6. These data suggest that β-MSH or peptides containing β-MSH may play a role in the regulation of aldosterone secretion during sodium depletion in the rat and that β-MSH increases aldosterone production partly by stimulating the late step in aldosterone biosynthesis, the conversion of corticosterone into aldosterone.

Changes in Vascular Ionic Composition at Different Stages of DOC-Salt Hypertension in the Rat

1981 ◽  
Vol 61 (1) ◽  
pp. 115-118 ◽  
Author(s):  
M. F. Villamil ◽  
C. Amorena ◽  
J. Ponce ◽  
A. Müller ◽  
A. C. Taquini
Keyword(s):  
Skeletal Muscle ◽  
Drinking Water ◽  
Potassium Chloride ◽  
Water Content ◽  
Ionic Composition ◽  
Single Mechanism ◽  
Inulin Space ◽  
Salt Hypertension ◽  
Ionic Changes ◽  
Total Sodium

1. Sequential changes in the ionic composition of the aorta and skeletal muscle were followed during 1, 2 and 4–6 weeks in 30 rats given deoxycorticosterone (DOC) and salt supplemented with potassium chloride. Twenty-one rats, drinking water, were used as controls. 2. Twenty-five per cent of the test rats were hypertensive after 1 week, 60% after 2 weeks and 100% after 4–6 weeks. 3. Muscle potassium fell in all test rats by an average of 15%. In contrast, aortic potassium fell by 19% only in those rats which did not develop hypertension after 1 week. 4. Total and non-inulin sodium and water of the aorta were normal in rats which remained normotensive after 1 or 2 weeks and high in those which became hypertensive during the same period. 5. Total sodium and water content of the aorta were also high in rats which were hypertensive at 4–6 weeks. However, because of simultaneous expansion of the inulin space, non-inulin fractions were normal in this group. 6. Results suggest that vascular ionic changes participate in the pathogenesis of DOC-salt hypertension through more than a single mechanism.

Investigations into the causes of the rise in aldosterone secretion during haemorrhage Part II

1966 ◽  
Vol 250 (767) ◽  
pp. 277-310
Keyword(s):  
Blood Loss ◽  
Constant Infusion ◽  
Necessary Condition ◽  
Posterior Lobe ◽  
Donor Blood ◽  
Aldosterone Secretion ◽  
Steroid Synthesis ◽  
Aldosterone Production ◽  
Secretion Rates

The role of ACTH and of renin as mediators of the stimulating effect of haemorrhage on aldosterone secretion was investigated. The following experiments showed that release of ACTH is not indispensible for the effect: in non-hypophysectomized dogs with intact kidneys, in which the blood ACTH concentration was artificially raised by infusing ACTH , there was still a rise in aldosterone production after blood loss. Hypophysectomy did not abolish or reduce the response, in fact, it increased its frequency of occurrence in dogs in which steroid synthesis was maintained at a submaximal level by a constant infusion of ACTH . Another group of studies demonstrated that the release of renin is also not a necessary condition for the rise in aldosterone production after bleeding; dogs in which both kidneys had been removed, but the pituitary left intact, responded to bleeding by a rise in aldosterone secretion of the same magnitude as normal dogs. However, in the simultaneous absence of kidneys and pituitary gland aldosterone production did not rise after bleeding although the basic conditions for synthesis of steroids were provided by a constant infusion of ACTH . On the contrary, severe falls in steroid secretion rates were the rule. These falls were attributed to the fact that hypophysectomized-nephrectomized dogs often reacted to blood loss with collapse of the circulation, and it was possible to argue that this collapse, and not the absence of kidney and pituitary, might have prevented the rise in aldosterone secretion. Attempts were therefore made to improve the circulation by supplying pressor substances known to be released in haemorrhage: of these noradrenaline did not improve the tolerance to haemorrhage, angiotensin improved it only very slightly, but prolonged infusions of extracts of posterior lobe restored it nearly to normal. In some of these experiments, the post-haemorrhage fall in aldosterone secretion was also prevented, but a rise was never seen. Aldosterone secretion of the hypophysectomized-nephrectomized dog was stimulated by infusion of large volumes of donor blood obtained from dogs with intact kidneys which presumably contains renin, but not of blood from nephrectomized donors. No evidence was obtained for the existence of agents other than ACTH and angiotensin as mediators of the stimulating effect of haemorrhage on aldosterone secretion. Furthermore, these two agents could fully replace each other, as shown by the finding that the effect of haemorrhage was not diminished by either nephrectomy or hypophysectomy alone.

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