ALDOSTERONE STIMULATION IN VITRO

1965 ◽  
Vol 48 (2) ◽  
pp. 283-296 ◽  
Author(s):  
Jürg Müller
Keyword(s):  
Adrenal Glands ◽  
High Concentration ◽  
Deficient Diet ◽  
Small Doses ◽  
Aldosterone Production ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Double Isotope ◽  
Very High

ABSTRACT A method is described for assaying aldosterone-stimulating activity in vitro using adrenal glands of rats kept on a sodium deficient diet. The production of aldosterone and corticosterone was measured by double isotope dilution derivative assays. Addition of ACTH or precursor steroids and elevation of the potassium concentration in the incubation medium gave a significant increase of aldosterone production. Angiotensin II showed little aldosterone-stimulating activity and only at a very high concentration. Small doses of a purified extract from human urine lead to a reproducible, significant and dose-dependent increase of aldosterone production without influencing production of corticosterone. The theoretical and practical advantages and limitations of the method are evaluated.

STIMULATION OF ALDOSTERONE BIOSYNTHESIS IN VITRO BY SEROTONIN

1968 ◽  
Vol 59 (1) ◽  
pp. 23-35 ◽  
Author(s):  
Jürg Müller ◽  
Walter H. Ziegler
Keyword(s):  
Fluorescence Spectra ◽  
Retention Volume ◽  
Indole Derivatives ◽  
Rat Serum ◽  
Aldosterone Production ◽  
Other Substances ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Stimulation Of

ABSTRACT The dialysable fraction of rat serum, which was previously shown to stimulate aldosterone production in rat adrenal sections, was chromatographed on Sephadex G-25. Fluorescence spectra indicated that a 5-hydroxyindole derivative was present in the active eluate fraction. The aldosterone-stimulating activity of serum dialysate had a similar retention volume to serotonin and 5-hydroxytryptophan, but was separated from other indole derivatives. Addition of small amounts of pure serotonin to the incubation medium led to a significant and dose-dependent increase of aldosterone and deoxycorticosterone production but did not affect corticosterone production. At higher concentrations, 5-methoxytryptamine, bufotenine and 5-hydroxytryptophan also stimulated aldosterone biosynthesis, whereas a number of other substances chemically or pharmacologically related to serotonin were found to be inactive. Two different serotonin antagonists completely blocked the aldosterone-stimulating effects of serotonin and rat serum but did not influence aldosterone stimulation by ACTH. Serotonin stimulated the incorporation of tritiated cholesterol into aldosterone but not the incorporation of tritiated pregnenolone, indicating that it acts on the conversion of cholesterol to pregnenolone.

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.

Neonatal hypoxic hyperlipidemia in the rat: effects on aldosterone and corticosterone synthesis in vitro

2000 ◽  
Vol 278 (3) ◽  
pp. R663-R668 ◽  
Author(s):  
Hershel Raff ◽  
Eric D. Bruder ◽  
Barbara M. Jankowski ◽  
Theodore L. Goodfriend
Keyword(s):  
Fatty Acids ◽  
Adrenal Glands ◽  
Plasma Lipids ◽  
Plasma Cholesterol ◽  
Neonatal Rat ◽  
Nonesterified Fatty Acids ◽  
Aldosterone Production ◽  
Old Rats ◽  
In Cells

Neonatal hypoxia increases aldosterone production and plasma lipids. Because fatty acids can inhibit aldosterone synthesis, we hypothesized that increases in plasma lipids restrain aldosteronogenesis in the hypoxic neonate. We exposed rats to 7 days of hypoxia from birth to 7 days of age (suckling) or from 28 to 35 days of age (weaned at day 21). Plasma was analyzed for lipid content, and steroidogenesis was studied in dispersed whole adrenal glands untreated and treated to wash away lipids. Hypoxia increased plasma cholesterol, triglycerides, and nonesterified fatty acids in the suckling neonatal rat only. Washing away lipids increased aldosterone production in cells from 7-day-old rats exposed to hypoxia, but not in cells from normoxic 7-day-old rats or from normoxic or hypoxic 35-day-old rats. Addition of oleic or linolenic acid to washed cells inhibited both aldosterone and corticosterone production, although cells from hypoxic 7-day-old rats were less sensitive. We conclude that hypoxia induces hyperlipidemia in the suckling neonate and that elevated nonesterified fatty acids inhibit aldosteronogenesis.

THE SYNTHESIS OF DNA AND RNA IN HUMAN CARCINOMATOUS ENDOMETRIUM IN SHORT-TERM INCUBATION IN VITRO AND ITS RESPONSE TO OESTRADIOL AND PROGESTERONE

1970 ◽  
Vol 48 (1) ◽  
pp. 29-38 ◽  
Author(s):  
S. NORDQVIST
Keyword(s):  
Nucleic Acids ◽  
Dna Synthesis ◽  
High Concentration ◽  
Short Term ◽  
Younger Women ◽  
Dna And Rna ◽  
Poorly Differentiated ◽  
Endometrial Carcinomas ◽  
Dose Dependent

SUMMARY Twenty-five endometrial carcinomas and three non-endometrial carcinomas were studied for the influence of various steroid hormones on the synthesis of DNA and RNA in short-term incubations in vitro. Endometrial carcinomas showed a dose-dependent sensitivity to progesterone in vitro, the response in both nucleic acids sometimes exceeding that of normal endometria. The mean reduction in DNA synthesis was to 46% and in RNA synthesis to 39% of the control values. Poorly differentiated carcinomas showed higher values of DNA synthesis than highly differentiated ones, as did carcinomas from younger women compared with those from older women. The response in vitro to progesterone was not correlated with these factors. Pregnenolone and a synthetic progestogen were less effective in vitro than progesterone. Oestradiol at a high concentration (20 μg/ml) in some cases significantly reduced the synthesis of both nucleic acids, possibly because of a specific 'toxic' action on the cells. No hormonal effects were observed in non-endometrial carcinomas.

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.

Cardiac effects of injections of epinephrine into the spinal intermediolateral column

1993 ◽  
Vol 265 (2) ◽  
pp. H633-H641 ◽  
Author(s):  
V. K. Malhotra ◽  
A. Kachroo ◽  
H. N. Sapru
Keyword(s):  
Adrenergic Receptors ◽  
Cardiovascular Responses ◽  
Spinal Level ◽  
Cardiac Effects ◽  
Alpha Adrenergic Receptors ◽  
Small Doses ◽  
The Right ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Stimulation Of

Small doses of epinephrine (0.008, 0.05, and 0.1 pmol, i.e., 20-nl volumes of 0.40, 2.5, and 5 microM solutions) produced a dose-dependent increase in heart rate when micro-injected into the right intermediolateral column (IML) at T2 spinal level. These effects were mediated via alpha 1-adrenergic receptors because prazosin blocked them. The presence of alpha 1-adrenergic receptors at this site was confirmed by microinjections of phenylephrine (a specific agonist for these receptors); phenylephrine elicited tachycardia. Larger doses of epinephrine (320, 2,000, and 3,200 pmol, i.e., 20-nl volumes of 16, 100, and 160 mM solutions) caused bradycardia when microinjected into the IML. These effects were mediated via alpha 2-adrenergic receptors because idazoxan blocked them. The presence of alpha 2-adrenergic receptors at this site was confirmed by microinjections of clonidine (a specific agonist for these receptors); clonidine elicited bradycardia. Injections of the vehicle (20 nl of normal saline containing 0.3% ascorbic acid, pH 7.4) did not evoke a response. Epinephrine, prazosin, or idazoxan did not alter the responses to L-glutamate. None of the doses of epinephrine elicited any response when injected intravenously. The aforementioned results provide pharmacological evidence for the presence of alpha 1- and alpha 2-adrenergic receptors in the IML at T2. Thus a basis is provided for investigating the role, if any, of alpha-adrenergic receptors in the IML in mediating cardiovascular responses elicited by the stimulation of different brain stem areas.

Stimulation of HCO3- transport in isolated proximal bullfrog duodenum by prostaglandins

1980 ◽  
Vol 239 (3) ◽  
pp. G198-G203 ◽  
Author(s):  
G. Flemstrom
Keyword(s):  
Electrical Potential ◽  
Potential Difference ◽  
Electrical Potential Difference ◽  
Morphological Examination ◽  
Minimal Concentration ◽  
Dependent Transport ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Stimulation Of

An in vitro preparation of proximal duodenum from the bullfrog transported alkali into the luminal solution (approximately 1 mueq x h-1 x cm-2) and generated a transepithelial electrical potential difference (5-10 mV, lumen negative). Transport was inhibited by 2,4-dinitrophenol (10(-5) M), CN- (5 X 10(-3) M), indomethacin (5 X 10(-5) M), and acetazolamide (5 X 10(-3) M) indicating that metabolism is required. Both alkali transport and the electrical potential difference showed a dose-dependent increase on administration of the prostaglandins E2, 16,16-dimethyl E2, and F2 alpha. The minimal concentration stimulating transport was lower with the E-type prostaglandins (10(-8) M than with F2 alpha (10(-6) M), and the former also produced greater maximal responses. In addition to metabolic-dependent transport of alkali, there was passive transmucosal migration of HCO3-, amounting to approximately 40% of basal (unstimulated) transport and sensitive to variation of the transmucosal hydrostatic pressure. Morphological examination showed that the preparation is devoid of Brunner glands. Stimulation of duodenal epithelial HCO3- transport by prostaglandins may contribute to their previously demonstrated ability to prevent duodenal ulceration.

Metabolic and Pharmacologic Interaction of Ethanol and Metronidazole in the Rat

1972 ◽  
Vol 50 (6) ◽  
pp. 476-484 ◽  
Author(s):  
H. Kalant ◽  
A. E. LeBlanc ◽  
M. Guttman ◽  
J. M. Khanna
Keyword(s):  
Incidental Finding ◽  
Repeated Administration ◽  
Volatile Material ◽  
Alcohol Dehydrogenase Activity ◽  
Liver Homogenates ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Concentration Curves ◽  
Central Depressant

Metronidazole, added in vitro, did not act either as an inhibitor or as a substrate for the alcohol dehydrogenase activity of rat liver homogenates. Concentration curves of ethanol and acetaldehyde in the blood after an oral dose of ethanol were not altered by pretreatment with metronidazole; in contrast, disulfiram caused marked elevation of acetaldehyde levels. When given once only, metronidazole (or possibly a metabolite of it) exerted a mild central depressant effect of its own and produced a dose-dependent increase in the intoxicant effect of ethanol. After repeated administration of metronidazole, synergism with ethanol was not seen. An incidental finding was the production of a volatile material during incubation of solutions containing NAD, which gives an acetone-like peak in gas-liquid chromatograms.

scholarly journals Effect of glucose on fermentation heat in sheep rumen fluid in vitro

1986 ◽  
Vol 56 (1) ◽  
pp. 305-311 ◽  
Author(s):  
A. Arieli
Keyword(s):  
Heat Production ◽  
High Glucose ◽  
Infinite Dilution ◽  
Rumen Fluid ◽  
Heat Production Rate ◽  
Sheep Rumen ◽  
Effect Of Glucose ◽  
Dose Dependent Increase ◽  
Dose Dependent

1. Heat production rate (H) of rumen fluid was measured in a direct calorimeter, Basal H of samples of 15 ml rumen fluid mixed with 45 ml buffer was 0.4 mW/ml rumen fluid.2. Addition of glucose (0.4–6.4 mg/sample) was followed by a dose-dependent increase in H. Maximal H was 1.1 rnW/ml and lasted up to 5 min, returning thereafter to the basal level.3. Expression of fermentation heat (Hf; kJ/mol substrate added) against glucose dose indicated an asymptotic dose response.4. Maximal Hf(at infinite dilution) agreed with stoichiometric calculations whereas minimal Hfsuggested a partial fermentation of the substrate at a high-glucose dose in the rumen environment.

Sign in / Sign up

Export Citation Format

Share Document