Hypothalamic cyclic AMP after the injection of ovarian steroids into ovariectomized rats

1989 ◽  
Vol 67 (4) ◽  
pp. 322-325 ◽  
Author(s):  
P. Zubin ◽  
S. Taleisnik
Keyword(s):  
Blocking Agent ◽  
Estradiol Benzoate ◽  
Ovariectomized Rats ◽  
Dependent Manner ◽  
Camp Concentration ◽  
Synthesis Inhibitor ◽  
Ovarian Steroids ◽  
Receptor Sites ◽  
Β Receptor ◽  
Dose Dependent

The effect of ovarian steroids on the concentration of adenosine 3′,5′ -cyclic monophosphate (c AMP) in the hypothalamus was studied in ovariectomized rats. Ovariectomized rats exhibited a lower cAMP concentration than intact rats. The administration of a single dose of estradiol benzoate (50 μg/kg body weight) resulted 3 days later in a rise of cAMP values, but levels did not reach those observed in estrous rats. Progesterone (2 mg/rat) injected 3 days after the priming dose of estradiol benzoate produced 4 h later no further changes in hypothalamic cAMP. The changes in hypothalamic cAMP concentration induced by estrogen treatment depend, at least in part, on noradrenergic inputs, since they were prevented by the injection of the norepinephrine synthesis inhibitor, diethyldithiocarbamate. In addition, administration of the β-blocking agent, propranolol, to estradiol- and estradiol–progesterone-treated rats lowered the concentration of cAMP in the hypothalamus in a dose-dependent manner. In contrast, the administration of an α-blocking agent, phenoxybenzamine, had no effect at the tested concentration. The results of this study indicate that estrogen increases cAMP concentration in the hypothalamus by a noradrenergic mechanism involving β-receptors. Moreover, the findings suggest that estrogen induces an increase in the number of β-receptor sites, whereas progesterone increases the apparent propranolol sensitivity for these receptor sites.Key words: cAMP, hypothalamus, ovarian steroids, adrenergic receptors, propranolol.

Meclofenamate inhibits prostaglandin E binding and adenylyl cyclase activation in human myometrium

1991 ◽  
Vol 129 (3) ◽  
pp. 439-445 ◽  
Author(s):  
A. López Bernal ◽  
S. Buckley ◽  
C. M. P. Rees ◽  
J. M. Marshall
Keyword(s):  
Inhibitory Effect ◽  
Human Myometrium ◽  
Prostaglandin E ◽  
Dependent Manner ◽  
Synthesis Inhibitor ◽  
Traditional Role ◽  
Mechanism Of Inhibition ◽  
Receptor Sites ◽  
Competitive Mechanism ◽  
Dose Dependent

ABSTRACT The effect of sodium meclofenamate on the binding of [3H]prostaglandin E2 ([3H]PGE2) to membranes from human myometrium was investigated. Meclofenamate inhibited the binding of [3H]PGE2 to high-affinity (dissociation constant 1·5 nmol/l) sites in a reversible dose-dependent manner (inhibition constant 11 μmol/l). The mechanism of inhibition was mainly competitive, but at high doses of meclofenamate (≥ 100 μmol/l) there was loss of PGE receptor sites. Of several PG synthesis inhibitors tested, only meclofenamate and, to a lesser extent, mefenamic acid had a significant inhibitory effect. PGE2 stimulated cyclic AMP generation in slices of human myometrium and this was inhibited by meclofenamate in a dose-dependent manner (50% inhibition occurred at 9 μmol/l). Again, this effect was specific for meclofenamate and fitted a competitive mechanism at doses in the range 1–10 μmol/l and a non-competitive mechanism at higher doses. The data show that meclofenamate, in addition to its traditional role as a PG synthesis inhibitor, affects directly PGE receptor binding and activation. Journal of Endocrinology (1991) 129, 439–445

scholarly journals Human chorionic gonadotropin regulates gastric emptying in ovariectomized rats

2012 ◽  
Vol 216 (3) ◽  
pp. 307-314 ◽  
Author(s):  
Kok-Min Seow ◽  
Jyun-Lin Lee ◽  
Ming-Luen Doong ◽  
Seng-Wong Huang ◽  
Jiann-Loung Hwang ◽  
...  
Keyword(s):  
Gastric Emptying ◽  
Chorionic Gonadotropin ◽  
Human Chorionic Gonadotropin ◽  
Gastrointestinal Transit ◽  
First Trimester ◽  
Dose Effect ◽  
Ovariectomized Rats ◽  
Dependent Manner ◽  
Ovx Rats ◽  
Dose Dependent

Prolongation of gastrointestinal transit resulting in nausea and vomiting in pregnancy (NVP) is the most common phenomenon during the first trimester of pregnancy. Increased human chorionic gonadotropin (hCG) concentration during the first trimester is the most likely cause of NVP. The aim of this study was to investigate the effect of hCG on gastrointestinal transit and plasma concentrations of cholecystokinin (CCK) in ovariectomized (Ovx) rats. I.p. injection of hCG was used to evaluate the dose effect of hCG on gastrointestinal transit in Ovx rats. The CCK antagonist lorglumide was used to clarify the role of CCK in regulating gastrointestinal transit. Gastrointestinal transit was assessed 15 min after intragastric gavage of a mixture of 10% charcoal and Na251CrO4(0.5 μCi/ml). After i.p. administration of hCG, gastric emptying was inhibited in Ovx rats, but intestinal transit was not affected. Plasma CCK concentrations were increased in a dose-dependent manner after hCG treatment, and gastric emptying showed a significant negative correlation with CCK concentrations (P=0.01,r2=−0.5104). Peripheral administration (i.p.) of lorglumide, a selective CCK1receptor antagonist, attenuated the hCG-induced inhibition of gastric emptying in Ovx rats, whereas central administration via the i.c.v. route did not. hCG treatment of Ovx rats inhibits gastric emptying in a dose-dependent manner via a peripheral mechanism of CCK hypersecretion and activation of CCK1receptors.

scholarly journals Methanolic Extract of Ceplukan Leaf (Physalis minimaL.) Attenuates Ventricular Fibrosis through Inhibition of TNF-αin Ovariectomized Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Bayu Lestari ◽  
Nur Permatasari ◽  
Mohammad Saifur Rohman
Keyword(s):  
Heart Failure ◽  
Treatment Group ◽  
Wistar Rats ◽  
Methanolic Extract ◽  
Ovariectomized Rats ◽  
Dependent Manner ◽  
Estrogen Level ◽  
Menopausal Women ◽  
Ventricular Fibrosis ◽  
Dose Dependent

The increase of heart failure prevalence on menopausal women was correlated with the decrease of estrogen level. The aim of this study is to investigate the effects of ceplukan leaf (Physalis minimaL.), which contains phytoestrogen physalin and withanolides, on ventricular TNF-αlevel and fibrosis in ovariectomized rats. Wistar rats were divided into six groups (control (—); OVX 5: 5-week ovariectomy (OVX); OVX 9: 9-week ovariectomy; treatments I, II, and III: 9-weeks OVX + 4-week ceplukan leaf’s methanolic extract doses 500, 1500, and 2500 mg/kgBW, resp.). TNF-αlevels were measured with ELISA. Fibrosis was counted as blue colored tissues percentage using Masson’s Trichrome staining. This study showed that prolonged hypoestrogen increases ventricular fibrosis (p<0.05). Ceplukan leaf treatment also resulted in a decrease of ventricular fibrosis and TNF-αlevel in dose dependent manner compared to without treatment group (p<0.05). Furthermore, the TNF-αlevel was normalized in 2500 mg/kgBWPhysalis minimaL. (p<0.05) treatment. The reduction of fibrosis positively correlated with TNF-αlevel (p<0.05,r=0.873). Methanolic extract of ceplukan leaf decreases ventricular fibrosis through the inhibition of ventricular TNF-αlevel in ovariectomized rats.

Lipoic acid stimulates bone formation in ovariectomized rats in a dose-dependent manner

2016 ◽  
Vol 94 (9) ◽  
pp. 947-954 ◽  
Author(s):  
Radoslaw Piotr Radzki ◽  
Marek Bienko ◽  
Dariusz Wolski ◽  
Alicja Lis ◽  
Agnieszka Radzka
Keyword(s):  
Body Mass ◽  
Lipoic Acid ◽  
Experimental Treatment ◽  
Physiological Saline ◽  
Ovariectomized Rats ◽  
Sham Operation ◽  
Dependent Manner ◽  
Skeletal Density ◽  
Female Wistar Rats ◽  
Dose Dependent

This study was undertaken to determine the osteotropic effect of different doses of lipoic acid (LA) on the mineralization of bone tissue in female Wistar rats with experimental osteopenia induced by bilateral ovariectomy. Fifty-six rats were randomly selected and submitted to either a sham operation (n = 8) or an ovariectomy (n = 48). The ovariectomized rats were randomly placed into two control groups, treated subcutaneously with either physiological saline or 17β-estradiol in the dose of 4 μg/kg body mass per day, and four experimental groups that received LA subcutaneously in the doses of 12.5, 25, 50, and 100 mg/kg body mass per day (n = 8 in each group). After 28 days of experimental treatment, the rats were sacrificed, and body mass, total skeletal density, and body composition were recorded. Blood serum and isolated femora were stored for further analysis. Our results revealed that the osteoprotective effect of LA was dose-dependent and was observed in rats treated with 50 and 100 mg/kg of LA. Moreover, the LA applied to the ovariectomized rats in the dose of 50 mg/kg not only stopped the bone resorption, but stimulated its formation.

Mechanisms of signal transduction for adenosine and ATP in pulmonary vascular bed

1992 ◽  
Vol 262 (3) ◽  
pp. H926-H929 ◽  
Author(s):  
H. L. Lippton ◽  
Q. Hao ◽  
T. Hauth ◽  
A. Hyman
Keyword(s):  
G Proteins ◽  
Purinergic Receptor ◽  
Blocking Agent ◽  
Dependent Manner ◽  
Vascular Bed ◽  
Vasoconstrictor Response ◽  
Txa2 Receptor Antagonist ◽  
Dose Dependent ◽  
Pulmonary Vascular Bed

The purpose of the present study was to investigate the contribution of pertussis toxin (PTX)-sensitive guanine nucleotide (G) proteins in the pulmonary vascular response to adenosine and ATP in the intact cat under conditions of controlled pulmonary blood flow and left atrial pressure. Adenosine, ATP, and beta-tau-ATP increased lobar arterial pressure in a dose-dependent manner. The pulmonary vasoconstrictor response to adenosine was abolished by BW 1433U, a specific purinergic receptor (P1) inhibitor, PTX pretreatment, indomethacin, and ONO 3708, a thromboxane A2 (TxA2) receptor antagonist. These data suggest that the pulmonary vasoconstrictor response to adenosine depends on activation of P1 purinergic receptors coupled to PTX-sensitive G proteins and subsequent metabolism of liberated arachidonic acid to form TxA2. Because each blocking agent studied produced similar reductions in the pulmonary vasoconstrictor response to ATP without altering the pulmonary vasoconstrictor response to beta-tau-ATP, the present data suggest that ATP constricts the pulmonary vascular bed, in part, by hydrolysis to adenosine. Moreover, the present study suggests that both A1 purinoceptors that are linked to PTX-sensitive G proteins as well as P2x purinoceptors receptors that are independent of PTX-insensitive G proteins mediate the pulmonary vasoconstrictor response to ATP in vivo.

Regulation of renal Na+-K+-ATPase in the rat by adrenal steroids

1981 ◽  
Vol 241 (2) ◽  
pp. F186-F195
Author(s):  
H. J. Rodriguez ◽  
S. K. Sinha ◽  
J. Starling ◽  
S. Klahr
Keyword(s):  
Dose Range ◽  
Dependent Manner ◽  
Adrenal Steroids ◽  
Electrolyte Excretion ◽  
Clear Cut ◽  
Renal Gluconeogenesis ◽  
Receptor Sites ◽  
Dose Dependent ◽  
Stimulation Of

The effects of single and multiple injections of aldosterone and dexamethasone on renal Na+-K+-ATPase, in vitro renal gluconeogenesis, and urinary electrolyte excretion were examined in adrenalectomized rats in a dose-dependent manner. Single maximal and supramaximal doses of aldosterone (defined by the effect of electrolyte excretion) had no effect on Na+-K+-ATPase or gluconeogenesis. By contrast, a single administration of dexamethasone (in a dose range that increased fasting blood sugar, stimulated renal gluconeogenesis, and had no mineralocorticoid effects) yielded clear-cut activation of Na+-K+-ATPase. Multiple submaximal doses of dexamethasone produced quantitatively similar stimulation of Na+-K+-ATPase and gluconeogenesis. Multiple supramaximal doses of aldosterone stimulated Na+-K+-ATPase and gluconeogenesis, but maximal and submaximal doses of the hormone were without effect. Aldosterone had no effect on hepatic Na+-K+-ATPase or gluconeogenesis. These results suggest that activation of renal Na+-K+-ATPase can be considered a putative glucocorticoid (not mineralocorticoid) effect. Renal Na+-K+-ATPase activation by chronic aldosterone treatment may be mediated by glucocorticoid receptor sites and, hence, may not represent a genuine mineralocorticoid effect.

scholarly journals Ovarian Steroids Stimulate Adenosine Triphosphate-Sensitive Potassium (KATP) Channel Subunit Gene Expression and Confer Responsiveness of the Gonadotropin-Releasing Hormone Pulse Generator to KATP Channel Modulation

Endocrinology ◽  
2008 ◽  
Vol 149 (5) ◽  
pp. 2423-2432 ◽  
Author(s):  
Wenyu Huang ◽  
Maricedes Acosta-Martínez ◽  
Jon E. Levine
Keyword(s):  
Gene Expression ◽  
Katp Channel ◽  
Pulse Generator ◽  
Katp Channels ◽  
Ovariectomized Rats ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Ovarian Steroids ◽  
Gnrh Secretion ◽  
Steroid Dependent

The ATP-sensitive potassium (KATP) channels couple intracellular metabolism to membrane potential. They are composed of Kir6.x and sulfonylurea receptor (SUR) subunits and are expressed in hypothalamic neurons that project to GnRH neurons. However, their roles in regulating GnRH secretion have not been determined. The present study first tested whether KATP channels regulate pulsatile GnRH secretion, as indirectly reflected by pulsatile LH secretion. Ovariectomized rats received sc capsules containing oil, 17β-estradiol (E2), progesterone (P), or E2+P at 24 h before blood sampling. Infusion of the KATP channel blocker tolbutamide into the third ventricle resulted in increased LH pulse frequency in animals treated with E2+P but was without effect in all other groups. Coinfusion of tulbutamide and the KATP channel opener diazoxide blocked this effect, whereas diazoxide alone suppressed LH. Effects of steroids on Kir6.2 and SUR1 mRNA expression were then evaluated. After 24hr treatment, E2+P produced a modest but significant increase in Kir6.2 expression in the preoptic area (POA), which was reversed by P receptor antagonism with RU486. Neither SUR1 in the POA nor both subunits in the mediobasal hypothalamus were altered by any steroid treatment. After 8 d treatment, Kir6.2 mRNA levels were again enhanced by E2+P but to a greater extent in the POA. Our findings demonstrate that 1) blockade of preoptic/hypothalamic KATP channels produces an acceleration of the GnRH pulse generator in a steroid-dependent manner and 2) E2+P stimulate Kir6.2 gene expression in the POA. These observations are consistent with the hypothesis that the negative feedback actions of ovarian steroids on the GnRH pulse generator are mediated, in part, by their ability to up-regulate KATP channel subunit expression in the POA.

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