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.

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.

Heparin Induces Synthesis and Secretion of Tissue Factor Pathway Inhibitor from Endothelial Cells In Vitro

2000 ◽  
Vol 83 (06) ◽  
pp. 937-943 ◽  
Author(s):  
Birgit Svensson ◽  
Randi Olsen ◽  
Mirella Ezban ◽  
Bjarne Østerud ◽  
Ruth Paulssen ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Surface Membrane ◽  
Molecular Size ◽  
Fold Increase ◽  
Coagulation System ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Stimulation Of

SummaryTFPI is a potent inhibitor of the extrinsic coagulation system constitutively synthesized by endothelial cells. A major portion of intravascular TFPI is stored associated with endothelial cells, and administration of unfractionated heparin (UFH) in vivo causes a prompt mobilization of TFPI into the circulation. The present study was conducted to investigate how UFH affected the synthesis, secretion and anticoagulant potency of TFPI in endothelial cells in vitro. A spontaneously transformed immortal endothelial cell line was used (ECV304). Stimulation of ECV304 cells with UFH caused a prompt dose-dependent (0-5 IU UFH/ml) release of TFPI to the medium accompanied by no change of TFPI at the surface membrane assessed by immunocytochemical methods. Northern blot analysis revealed two mRNA transcripts for TFPI with a molecular size of 1.4 kb and 4.4 kb, respectively. Stimulation of ECV304 cells for 24 hrs with various concentrations of UFH caused a dose-dependent increase of TFPI in the medium (6.2-29.6 ng/106 cells within the concentration range 0-10 IU/ml). A similar dose-dependent increase in the expression of both TFPI mRNA species was observed. Long-term incubation of ECV304 cells with 5.0 IU/ml UFH caused a 5-10 fold increase in the TFPI concentration accumulated in the medium over 48 hrs. The increased TFPI mRNA expression induced by UFH appeared already after 10 min, peaked after 2-4 hrs, remained augmented throughout the entire period of UFH exposure, and preceeded the synthesis-dependent increase in TFPI release by 2-4 hrs. The procoagulant activity of the cells was downregulated by 36 % and the contribution of TFPI to the anticoagulant potency of ECV304 cells was moderately increased after 24 hrs heparin stimulation. It is suggested that these mechanisms are of major importance for the anticoagulant function of heparins.

Cholera toxin stimulates secretion of immunoreactive intestinal mucin

1981 ◽  
Vol 240 (1) ◽  
pp. G10-G16 ◽  
Author(s):  
J. F. Forstner ◽  
N. W. Roomi ◽  
R. E. Fahim ◽  
G. G. Forstner
Keyword(s):  
Cholera Toxin ◽  
Mucin Secretion ◽  
Glycoprotein Synthesis ◽  
Intestinal Mucin ◽  
Storage Granules ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Stimulation Of

In vitro secretion of goblet cell mucin from rat small intestine was measured using a double-antibody radioimmunoassay for mucin. Cholera toxin (12.5-50 mg crude filtrate/ml) added to incubations of intestinal slices caused a dose-dependent increase in mucin secretion. By 90 min there was a four- to fivefold enhancement in secretion over noncholera-treated controls. Crude filtrate (dialyzed or nondialyzed) was a more effective mucin secretogogue than purified enterotoxin. Secretion was also assessed by administering [1-14C]glucosamine intraperitoneally to rats in vivo and 3 h later monitoring in vitro secretion of radioactive glycoprotein from intestinal slices. Cholera filtrate (12.5-50 mg/ml) caused a 1.5- to 2.0-fold enhancement in secretion after 90 min. The radioactivity data, however, underestimated total mucin secretion and the dependency of secretion on the dose of cholera filtrate. Cholera preparations also caused an enhancement (20-30% over controls) in the incorporation of [3H]glucosamine into tissue acid-precipitable glycoprotein, indicating a stimulation of glycoprotein synthesis. In the same experiments it was noted that the secretion of 3H-labeled (i.e., newly glycosylated) glycoprotein was increased 2.5- to 3.0-fold over untreated controls. Assuming that radioactivity partially reflects mucin synthetic and secretory events, it is possible, therefore, that cholera toxin promotes the release of both "old" mucin from storage granules as well as the synthesis and secretion of "new" mucin formed in goblet cells during incubation.

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.

Mediation of muscarinic stimulation of pepsinogen secretion in the frog

1985 ◽  
Vol 248 (1) ◽  
pp. G79-G86
Author(s):  
M. Inoue ◽  
J. Fong ◽  
G. Shah ◽  
B. I. Hirschowitz
Keyword(s):  
In Vitro Release ◽  
Free Medium ◽  
American Bullfrog ◽  
Pepsinogen Secretion ◽  
Improved Model ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Vitro Release ◽  
Stimulation Of

The in vitro release of pepsinogen secretion by the isolated esophagus of the American bullfrog was studied with an improved model system. The tissue was mounted in a double chamber that preserves mucosal polarity and provides both control and test segments, each 1 cm2 from the same tissue. Pepsinogen secretion was severalfold higher than previously found with mucosal strips and could be sustained for several hours. Bethanechol (BCh) caused concentration-dependent (0.1-50 microM) pepsinogen secretion with a Vmax of 74 +/- 12 micrograms X mg prot-1 X h-1 or 50-60% of total pepsinogen; Km was 3 microM and 500 microM BCh stimulated at less than the Vmax value. Atropine specifically blocked BCh and pA2 = 9.3. In the presence of 100 microM isobutylmethyxanthine, BCh produced a dose-dependent increase in tissue cAMP but not cGMP. BCh remained effective in Ca2+-free medium. In calcium-free medium EGTA concentration dependently (0.2-5 mM) suppressed the pepsinogen response to BCh. The evidence thus far suggests that cholinergic stimulation of pepsinogen secretion in the tissue acts via both cAMP and Ca2+. More specific studies would be required for absolute confirmation of either or both apparent mechanisms and to resolve how they interact.

Stimulation of Aldosterone Production in vitro by Ammonium Ions

Nature ◽  
1965 ◽  
Vol 206 (4979) ◽  
pp. 92-92 ◽  
Author(s):  
JüRG MüLLER
Keyword(s):  
Ammonium Ions ◽  
Aldosterone Production ◽  
Stimulation Of

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.

Antral gland cell column: a method for studying release of gastric hormones

1983 ◽  
Vol 245 (4) ◽  
pp. G463-G469
Author(s):  
B. Richelsen ◽  
J. F. Rehfeld ◽  
L. I. Larsson
Keyword(s):  
In Vitro Release ◽  
Dependent Manner ◽  
Gastrin Release ◽  
Cell Column ◽  
Independent Manner ◽  
Response Characteristics ◽  
Dose Dependent ◽  
Vitro Release ◽  
Stimulation Of

A technique for studying in vitro release of gastric hormones has been developed. The system utilizes nonenzymatically isolated antropyloric glands from humans or rats, which are perifused in a Bio-Gel P-2 column. The system permits the study of kinetics and dose-response characteristics using the glands as their own control. The glands were stimulated with carbachol and bombesin, and the antral peptides gastrin and somatostatin were measured. Bombesin and carbachol both evoked a dose-dependent stimulation of gastrin release, beginning at below 10(-10) M (bombesin) and 10(-7) M (carbachol). Carbachol inhibited the release of somatostatin in a dose-dependent manner, being maximally effective at 10(-6) M and then producing 60% inhibition of somatostatin release. Bombesin was without effect on antropyloric somatostatin release. These data suggest that the gastrin-stimulating effect of carbachol is partially or totally due to inhibition of somatostatin release, whereas bombesinergic stimulation of gastrin release must work in an independent manner. In addition, data on the effects of these substances on the release of gastrin and ACTH-like peptides from human antropyloric glands are presented. Due to the absence of local neural reflexes, this system is a useful supplement to the isolated perfused stomach model.

Stimulation of acetylcholine release in myenteric plexus by calcitonin gene-related peptide

1990 ◽  
Vol 259 (6) ◽  
pp. G934-G939 ◽  
Author(s):  
M. W. Mulholland ◽  
S. Jaffer
Keyword(s):  
Myenteric Plexus ◽  
Acetylcholine Release ◽  
Calcitonin Gene Related Peptide ◽  
Ach Release ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Dependent Mechanism ◽  
Stimulation Of

The effects of calcitonin gene-related peptide (CGRP) on acetylcholine (ACh) release from myenteric plexus neurons in primary culture were investigated. CGRP (10(-12) to 10(-6) M) produced a dose-dependent increase in [3H]ACh release. The ACh release caused by CGRP was significantly inhibited (74 +/- 24%) by preincubation with dideoxyadenosine but was increased more than threefold by preincubation with theophylline. Incubation of myenteric plexus neurons with CGRP (10(-8) M) in the presence of diltiazem (10(-5) M) or in a calcium-free medium markedly reduced [3H]ACh release. CGRP potentiated [3H]ACh release stimulated by potassium or substance P but not by cholecystokinin octapeptide or forskolin. The results demonstrate that CGRP cause release of ACh from guinea pig myenteric plexus neurons and suggest that the peptide acts through an adenosine 3',5'-cyclic monophosphate-dependent mechanism that involves neuronal calcium channels.

Secretory patterns of 1α-hydroxycorticosterone in the isolated perifused interrenal gland of the dogfish, Scyliorhinus canicula

1990 ◽  
Vol 5 (1) ◽  
pp. 55-60 ◽  
Author(s):  
L. B. O'Toole ◽  
K.J. Armour ◽  
C. Decourt ◽  
N. Hazon ◽  
B. Lahlou ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Significant Rise ◽  
Dependent Manner ◽  
Steroid Production ◽  
Secretory Rate ◽  
Scyliorhinus Canicula ◽  
Interrenal Gland ◽  
Dose Dependent ◽  
Stimulation Of

ABSTRACT An isolated in-vitro perifused interrenal gland preparation from the dogfish Scyliorhinus canicula was used to study production of quantitatively the major corticosteroid 1α-hydroxycorticosterone (1α-OH-B), measured by radioimmunoassay. Basal secretory rates were 877·1 ± 145 (s.e.m.) fmol/mg per 15 min (n=14) and the preparation remained viable for up to 22 h, as reflected in a brisk response to 10 μm cyclic AMP (cAMP) after this time. Steroid production responded in a dose-dependent manner to porcine ACTH, with 10 μm producing a maximum stimulation of 225% above the basal secretory rate. cAMP (10 μm) produced an increase of 278% above basal, while 1 μm forskolin increased basal secretory rates by 127%. [Val5]- and [Ile5]-angiotensin II (0·1 μm) increased 1α-OH-B production by 120 and 372% respectively over basal secretory rates. Increasing the concentration of K+ in the perfusate from 8 mm to 12, 18, 28 and 40 mm produced a significant rise only at 28 mm. Alterations in the concentration of Na+ and osmolarity of the perifusion medium had inconsistent effects on steroid production. Increased concentrations of urea (from 360 to 720 mm) increased the basal secretory rate by 121%, whilst reducing the concentration of urea (from 360 to 90 mm) had no effect.

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