Estimation of the genetic activity of epinephrine hydrotartrate on the model of erythrocytes in peripheral blood in mice

2021 ◽  
Vol 1 (2) ◽  
pp. 6-10
Author(s):  
M. Ya. Ibragimova ◽  
◽  
S. Yu. Zaytsev ◽  
V. V. Semenov ◽  
◽  
...  
Keyword(s):  
Peripheral Blood ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Genetic Effects ◽  
Receptor Ligand ◽  
Antimutagenic Effect ◽  
Genetic Activity ◽  
Ad Libitum ◽  
And Control ◽  
Β Adrenergic Receptors

The aim of the study was to evaluate the genetic activity of erythrocytes in peripheral on the model of peripheral blood erythrocytes in mice. The studies were carried out on mice (males) of the C 57B4/6 line weighing 20 g (1,5–2 months of age). For each experimental and control variant, six males were taken. The animals were kept in vivarium conditions according to international criteria for rinofix bedding, food and water ad libitum. When determining the genetic effects, the adrenergic receptor ligand was injected subcutaneously once. After 8 hours, a mutation inducer, an alkylating drug, cyclophosphamide, was injected intraperitoneally at a dose of 30 mg/kg. Before the end of the experiment in 2,5 hour, mice were injected intraperitoneally with 2.5 mg/kg of colchicine. 24 hours after injection, the animals were euthanized by delongation. The number of erythrocytes with micronuclei was counted from 2000 analyzed cells. The greatest antimutagenic effect (87,5%) of epinephrine hydrotartrate, a stimulator of α- and β-adrenergic receptors, was found at doses of 5 and 0,5 mg/kg.

α-Adrenergic receptor modulation of the intrathoracic efferent sympathetic nervous system regulating the canine heart

1989 ◽  
Vol 67 (10) ◽  
pp. 1199-1204 ◽  
Author(s):  
J. A. Armour
Keyword(s):  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Blocking Agent ◽  
Sympathetic Ganglia ◽  
Canine Heart ◽  
Receptor Modulation ◽  
Adrenergic Antagonist ◽  
Cervical Ganglia ◽  
Β Adrenergic Receptors ◽  
Stimulation Of

The augmentation of ventricular inotropism induced by electrical stimulation of acutely decentralized efferent sympathetic preganglionic axons was reduced, but still present, following administraiton of hexamethonium (10 mg/kg i.v.). While hexamethonium continued to be administered, the cardiac augmentations so induced were enhanced significantly following administration of the α-adrenergic receptor blocking agent, phentolamine myselate (1 mg/kg i.v.). Stimulation of the sympathetic efferent postganglionic axons in cardiopulmonary nerves induced cardiac augmentations that were unchanged following administration of these agents singly or together. The cardiac augmentations induced by stimulation of efferent preganglionic sympathetic axons were unchanged when phentolamine was administered alone. The augmentations of cardiac inotropism induced by efferent postganglionic sympathetic axonal stimulation were decreased following local administration of the β-adrenergic antagonist timolol into the ipsilateral stellate and middle cervical ganglia. Thereafter, these augmentations were unchanged following the subsequent intravenous administration of phentolamine. It is concluded that the activation of cardiac neurons in the stellate and middle cervical ganglia by stimulation of efferent preganglionic sympathetic axons can be modified by α-adrenergic receptors and that these effects are dependent upon β-adrenergic receptors, not nicotinic ones, in intrathoracic ganglia.Key words: α-adrenergic inotropism, sympathetic ganglia, hexamethonium, phentolamine.

scholarly journals Thyroid-hormone modulation of the number of β-adrenergic receptors in rat fat-cell membranes

1978 ◽  
Vol 176 (3) ◽  
pp. 1007-1010 ◽  
Author(s):  
Y Giudicelli
Keyword(s):  
Thyroid Hormone ◽  
Binding Sites ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Receptor Density ◽  
Beta Adrenergic Receptors ◽  
Fat Cell ◽  
Beta Adrenergic ◽  
Hormone Modulation ◽  
Β Adrenergic Receptors

Adipocytes from thyroidectomized rats contain 3 times less [3H]dihydroalprenolol-binding sites (beta-adrenergic receptors) than adipocytes from euthyroid animals. This alteration is not solely due to cell-size differences, but also to a thyroidectomy-induced defect in beta-adrenergic receptor density per adipocyte surface area, a defect that is furthermore corrected by tri-iodothyronine treatment.

scholarly journals INCREASED BETA2-ADRENERGIC RECEPTOR SIGNALING ENHANCES PROGRESSION OF HEPATOCELLULAR CARCINOMA

2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S106-S106
Author(s):  
Jason Pizzini ◽  
Hanzhou Wang ◽  
Chih-Ko Yeh ◽  
Amrita Kamat
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cardiovascular Diseases ◽  
Beta Blocker ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Beta Blockers ◽  
Therapeutic Option ◽  
Propranolol Treatment ◽  
Receptor Action ◽  
And Control

Abstract We investigated whether increased signaling by beta2-adrenergic receptors (β2-ARs), which mediate the action of catecholamines, enhances the progression of hepatocellular carcinoma (HCC). Mean age of patients with HCC, the most prolific form of liver cancer, has progressively increased over the last decade. Beta2-AR-mediated signaling in liver increases with age. We also observed increased β2-AR levels in liver tissues of patients with HCC compared to control subjects. We, therefore, hypothesized that increased β2-AR signaling enhances HCC progression while inhibition of β2-AR signaling by treatment with beta blockers suppresses its progression. To test this hypothesis, we used N-nitrosodiethylamine (DEN) to induce HCC in liver-specific β2-AR knockout (LKO) and control mice in the absence or presence of beta blocker propranolol. At the end of 25 weeks, we observed increased numbers of visible tumors, disarray of liver architecture, and mortality in DEN-induced control mice which was reduced by propranolol treatment. We also observed that DEN-treated LKO mice demonstrated reduced mortality, disarray of architecture, and phosphorylation of oncogene Src compared to DEN-treated control mice. Taken together, these results indicate that decreased β2-AR signaling because of a lack of receptors in the liver or inhibition of receptor action with propranolol reduces HCC progression. Studies are in progress to determine the β2-AR-mediated mechanisms involved in HCC progression. Our studies suggest that beta blocker propranolol, used to treat cardiovascular diseases, may be repurposed as a potential therapeutic option for treatment of HCC.

Regulation by progesterone of the high-affinity state of myometrial β-adrenergic receptor and of adenylate cyclase activity in the pregnant rat

1991 ◽  
Vol 6 (2) ◽  
pp. 137-145 ◽  
Author(s):  
J. Cohen-Tannoudji ◽  
V. Vivat ◽  
J. Heilmann ◽  
C. Legrand ◽  
J. P. Maltier
Keyword(s):  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Maximum Velocity ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Pregnant Rat ◽  
High Affinity ◽  
Β Adrenergic Receptors

ABSTRACT The effects of pregnancy or progesterone dominance on the β-adrenergic responsiveness of the uterus were studied in myometrial membranes from mid-and late-pregnant rats (day 15 and on the 16th h of day 22 of pregnancy respectively) or 24 h after administration of progesterone. Levels of the high (RH)- and low (RL)-affinity states of the β-adrenergic receptor were determined by competition experiments between 125I-labelled cyanopindolol binding and the selective β-agonist isoproterenol. The ratio KL/KH (respective dissociation constants) was determined since it also reflects the degree of formation of the high-affinity state of the β-adrenergic receptor. From day 15 to the 10th h of day 22 of pregnancy, two distinct affinity states were apparent: 80–55% RH (KH=0·31–0·21 μm) and 45–20% RL (KL=14–5 μm) with a ratio of KL/KH of 55–34. In the last 6 h before birth, β-adrenergic receptors underwent uncoupling which was paralleled by decreased responsiveness of myometrial adenylate cyclase to isoproterenol (maximum velocity (Vmax)=17±3 vs 44±3 fmol cyclic AMP/10 min per mg protein on day 15). At this stage of pregnancy, previous exposure to progesterone resulted in a 1·8-fold increase in 125I-labelled cyanopindolol-binding sites (Bmax) and the reappearance of the high-affinity state (67% RH, KH=0·19±0·04 (s.e.m.) μm, ratio KL/KH=81·1 ± 16·9). These results were reversed in the presence of the antiprogestin RU486 (100% RL, KL=24·6±4·1 μm, 41% reduction of Bmax). Moreover, after progesterone, adenylate cyclase activity was strongly stimulated by isoproterenol (Vmax=60±12 fmol cyclic AMP/10 min per mg protein vs 17±3 in controls). The data suggest (1) that progesterone may exert a permissive effect on β-adrenergic responsiveness of the pregnant rat myometrium and (2) that at term, both a desensitization mechanism involving uncoupling of β-adrenergic receptors and a decrease in activation of adenylate cyclase lead to a loss of myometrial response to β-agonists.

Trypsinization of bovine parathyroid cells abolishes Ca2+-regulated parathyroid hormone secretion

1989 ◽  
Vol 122 (1) ◽  
pp. 213-218 ◽  
Author(s):  
R. Muff ◽  
J. A. Fischer
Keyword(s):  
Protein Kinase C ◽  
Parathyroid Hormone ◽  
Protein Kinase ◽  
Adrenergic Receptors ◽  
Hormone Secretion ◽  
Dependent Manner ◽  
Kinase C ◽  
And Control ◽  
Β Adrenergic Receptors ◽  
Dose Dependent

ABSTRACT The secretion of parathyroid hormone (PTH) is inversely related to the extracellular Ca2+ concentration (Cae2+). To test the hypothesis that a Ca2+ sensor on the surface of parathyroid cells is involved in Ca2+-regulated PTH secretion, limited trypsinization of bovine parathyroid cells was carried out. Treatment with trypsin (1·1–10 mg/ml) inhibited, in a dose-dependent manner, PTH secretion stimulated by lowering Cae2+ from 2·0 to 0·5 mmol/l. In control cells, activation of protein kinase C with 12-O-tetradecanoylphorbol-13-acetate (TPA) enhanced PTH secretion at 2·0 mmol Cae2+/1 but not at 0·5 mmol Cae2+/1. In trypsinized cells, however, TPA enhanced PTH secretion at both 0·5 and 2·0 mmol Cae2+/1. Isoproterenol-stimulated PTH secretion was maintained in trypsinized cells, but reduced cyclic AMP production revealed that some β-adrenergic receptors were destroyed. The cytosolic free Ca2+ concentration (Cai2+), as measured with fura-2, was raised within seconds in response to increasing Cae2+ from 0·5 to 2·0 mmol/l and was then lowered within 1 min to a sustained plateau; the changes were the same in trypsinized and control cells. In conclusion, trypsinization of parathyroid cells abolished Ca2+-regulated PTH secretion without affecting Cai2+. Journal of Endocrinology (1989) 122, 213–218

Interaction between prolactin and catecholamines on hypothalamic GnRH release in vitro

1996 ◽  
Vol 151 (2) ◽  
pp. 269-275 ◽  
Author(s):  
A E Calogero ◽  
N Burrello ◽  
A M Ossino ◽  
R F A Weber ◽  
R D'Agata
Keyword(s):  
Receptor Antagonist ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Inhibitory Effect ◽  
Inhibitory Effects ◽  
Experimental Conditions ◽  
Adrenergic Mechanism ◽  
Gnrh Release ◽  
Β Adrenergic Receptors

Abstract Brain catecholamines have been implicated in the regulation of gonadotrophin release. It has been recently reported that noradrenaline (NA), applied within the hypothalamic paraventricular nucleus, suppresses the pulsatile release of LH in the rat through a corticotrophin-releasing hormone (CRH)-dependent mechanism. Prolactin (PRL) is also able to suppress hypothalamic GnRH release following activation of the CRH-releasing neurone. Given that PRL stimulates the release of NA from hypothalamic explants and that NA stimulates the release of hypothalamic CRH, we hypothesized that this neurotransmitter may be involved in the intrahypothalamic neuroendocrine circuit mediating the inhibitory effects of PRL on GnRH release. To test this hypothesis, we evaluated the effects of PRL on GnRH release in the presence of α- or β-adrenergic receptor antagonists using a static hypothalamic organ culture system which enabled us to evaluate immunoreactive GnRH (iGnRH) release from individually incubated, longitudinally halved hypothalami. As previously shown, PRL at a concentration of 100 nm inhibited basal iGnRH release by about 35%. Phentolamine, a non-selective α-adrenergic receptor antagonist, prazosin, an α1-receptor antagonist, and yohimbine, an α2-receptor antagonist, overcame the inhibitory effect of PRL on iGnRH release in a concentration-dependent fashion. In contrast, propranolol, a non-selective β-adrenergic receptor antagonist, atenolol, a β1-receptor antagonist, and ICI-118,551, a β2-receptor antagonist, had no effect. None of these compounds had any effect on basal iGnRH release. These findings suggested that an α-adrenergic mechanism is involved in the suppressive effects of PRL on GnRH release. Since the activation of α-adrenergic receptors increases hypothalamic CRH release, we evaluated whether PRL stimulates CRH release via an α-adrenergic mechanism. PRL stimulated basal CRH release by about twofold and this effect was inhibited by phentolamine in a concentration-dependent fashion. In conclusion, α-, but not β-, adrenergic receptors mediate the inhibitory effects of PRL on GnRH release in vitro. We speculate that, at least under these experimental conditions, PRL inhibits GnRH release through an α-adrenergic mechanism which activates the CRH-secreting neurone. Journal of Endocrinology (1996) 151, 269–275

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