Activation of Na+- and Ca2+-dependent Mg2+ extrusion by α1- and β-adrenergic agonists in rat liver cells

2000 ◽  
Vol 279 (5) ◽  
pp. G943-G950 ◽  
Author(s):  
Theresa E. Fagan ◽  
Andrea Romani
Keyword(s):  
Adrenergic Receptor ◽  
Liver Cells ◽  
Adrenergic Agonists ◽  
Experimental Conditions ◽  
Rat Liver Cells ◽  
Rat Livers ◽  
Cellular Ca ◽  
Adrenergic Receptor Agonist ◽  
Dependent Mechanism ◽  
Stimulation Of

The administration of selective α1 (phenylephrine)-, β (isoproterenol)-, or mixed (epinephrine) adrenergic agonists induces a marked Mg2+extrusion from perfused rat livers. In the absence of extracellular Ca2+, phenylephrine does not induce a detectable Mg2+ extrusion, isoproterenol-induced Mg2+mobilization is unaffected, and epinephrine induces a net Mg2+ extrusion that is lower than in the presence of extracellular Ca2+ and quantitatively similar to that elicited by isoproterenol. In the absence of extracellular Na+, no Mg2+ is extruded from the liver irrespective of the agonist used. Similar results are observed in perfused livers stimulated by glucagon or 8-chloroadenosine 3′,5′-cyclic monophosphate. In the absence of extracellular Na+ or Ca2+, adrenergic-induced glucose extrusion from the liver is also markedly decreased. Together, these results indicate that liver cells extrude Mg2+ primarily via a Na+-dependent mechanism. This extrusion pathway can be activated by the increase in cellular cAMP that follows the stimulation by glucagon or a specific β-adrenergic receptor agonist or, alternatively, by the changes in cellular Ca2+ induced by the stimulation of the α1-adrenoceptor. In addition, the stimulation of the α1-adrenoceptor appears to activate an auxiliary Ca2+-dependent Mg2+extrusion pathway. Finally, our data suggest that experimental conditions that affect Mg2+ mobilization also interfere with glucose extrusion from liver cells.

scholarly journals Effect of the α-agonist noradrenaline on total and 45Ca2+ movements in mitochondria of rat liver cells

1981 ◽  
Vol 200 (1) ◽  
pp. 177-180 ◽  
Author(s):  
Brigitte Berthon ◽  
Josiane Poggioli ◽  
Thierry Capiod ◽  
Michel Claret
Keyword(s):  
Rat Liver ◽  
Liver Cells ◽  
Isolated Cells ◽  
Experimental Conditions ◽  
Rat Liver Cells ◽  
Rat Livers ◽  
In Cells

Ca2+ movements triggered by noradrenaline were determined in isolated cells and mitochondria from rat livers. It has been shown that these depend on experimental conditions. In cells incubated in 1.8mm-Ca2+, results suggest that noradrenaline mobilizes Ca2+ from reticulum before releasing Ca2+ from mitochondria.

The content of nitric oxide and S-nitrosothiols in rats’ liver cells under the different supplementation of macronutrient

2020 ◽  
Vol 12 (2) ◽  
pp. 187-195
Author(s):  
Halyna Kopylchuk ◽  
Ivanna Nykolaichuk ◽  
Olesiia Kuziak
Keyword(s):  
Nitric Oxide ◽  
Nitrogen Oxide ◽  
Nitrosative Stress ◽  
Liver Cells ◽  
Oxide Content ◽  
Experimental Conditions ◽  
Before And After ◽  
Rat Liver Cells ◽  
Key Factor ◽  
Excessive Consumption

This paper presents studies of nitric oxide and low-molecular S-nitrosothiols in the mitochondrial and cytosolic fractions of the rats' liver under the conditions of, alimentary protein deprivation, consumption of excess sucrose content and combined action of two adverse factors. In order to model the low-protein diet of the animal for 28 days received an isocaloric diet containing 4.7% protein, 10% fat, 81,3% carbohydrates (starch – 37%, sucrose – 30%, cellulose – 5%) and was calculated in accordance with the recommendations of the American Institute of Nutrition. The high-sugar diet consisted of 14% protein, 10% fat, 72% carbohydrates (starch – 37%, sucrose – 30%, cellulose – 5%). The mitochondrial and cytosolic fraction of rat liver cells were obtained by the method of differential centrifugation. Nitrogen oxide content was assessed by a unified method by determining the NO2- content, which is a stable metabolite of nitric oxide. Since NO is inactivated into an oxidase reaction with the conversion into nitrite or nitrate that is quickly metabolized, the nitrogen oxide content was assessed by the change in NO2-. The concentration of S-nitrosothiols was recorded, respectively, by determining the concentration of nitrite anion before and after the addition of Hg2+ ions, which by modifying the S – N bonds catalyzes the release of S-nitrosyl thiols of nitric oxide. An increase in NO content in both hepatic subcellular fractions of the rats’ experimental groups compared to control values was found. However, a lack of protein in the diet (protein deficiency in the diet leads to an increase in nitric oxide levels in 3-4 times) can be considered as a key factor in the recorded changes in the mitochondria of the animals’ liver, while in the cytosol - excessive consumption of sucrose (3-5 times increase). Regarding the level of S-nitrosothiols, in the studied fractions, multidirectional changes in their concentration were found. Thus, an increase in the content of nitrosyl derivatives in the mitochondria of rat’s liver cells with a simultaneous decrease in their level in the cytosol indicates dysmetabolic disorders in the transport system and deposition of nitric oxide, which can lead to the development of nitrosative stress under the experimental conditions.

scholarly journals Actin and Vimentin proteins with N-terminal deletion detected in tumor-bearing rat livers induced by intraportal-vein injection of Ha-ras-transfected rat liver cells

2008 ◽  
Vol 124 (11) ◽  
pp. 2512-2519 ◽  
Author(s):  
Yasushi Nakamura ◽  
Akari Kominami ◽  
Yoshiyuki Tsujimoto ◽  
Yuko Nakayama ◽  
Tsukasa Kitahashi ◽  
...  
Keyword(s):  
Rat Liver ◽  
Liver Cells ◽  
Terminal Deletion ◽  
Tumor Bearing ◽  
Rat Liver Cells ◽  
Rat Livers

Oxytocin-induced renin secretion in conscious rats

2000 ◽  
Vol 278 (1) ◽  
pp. R226-R230 ◽  
Author(s):  
Wan Huang ◽  
Mats Sjöquist ◽  
Ole Skott ◽  
Edward M. Stricker ◽  
Alan F. Sved
Keyword(s):  
Receptor Antagonist ◽  
Adrenergic Receptor ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Renin Secretion ◽  
Systemic Injection ◽  
Angiotensin System ◽  
Conscious Rats ◽  
Adrenergic Receptor Agonist ◽  
Dependent Mechanism

Arterial hypotension and hypovolemia are known to stimulate neurohypophysial secretion of oxytocin (OT) in rats, although the physiological function of OT under these circumstances is uncertain. We now report that OT infused intravenously into conscious rats at 125 ng ⋅ kg−1 ⋅ h−1, a dose selected to mimic plasma OT levels during hypotension or hypovolemia, increased plasma renin concentration and plasma renin activity by twofold. This effect was prevented by systemic pretreatment with an OT receptor antagonist {[1-(3-mercaptopropionic acid)-2- O-ethyl-d-Tyr-Thr4-Orn8]-OT}. The OT antagonist did not block renin secretion induced by systemic injection of the β-adrenergic receptor agonist isoproterenol, indicating that the OT antagonist does not interfere nonselectively with renin release. Pretreatment of rats with the β-adrenergic receptor antagonist nadolol also prevented OT-induced renin secretion. Similarly, nadolol injected during infusion of OT markedly reduced the elevated plasma renin levels. These observations raise the possibility that pituitary OT secretion during hypotension or hypovolemia in rats may serve to support blood pressure by enhancing activation of the renin-angiotensin system via a β-adrenergic receptor-dependent mechanism.

scholarly journals The characteristics and site of inhibition of gluconeogenesis in rat liver cells by bacterial endotoxin. Stimulation of phosphofructokinase-1

1987 ◽  
Vol 242 (3) ◽  
pp. 721-728 ◽  
Author(s):  
R G Knowles ◽  
J P McCabe ◽  
S J Beevers ◽  
C I Pogson
Keyword(s):  
Enzyme Activities ◽  
Pyruvate Carboxylase ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Liver Cells ◽  
Atp Content ◽  
Rat Liver Cells ◽  
Endogenous Substrates ◽  
And Control ◽  
Control Coefficients ◽  
Stimulation Of

The characteristics and site of inhibition of gluconeogenesis by endotoxin were investigated in liver cells isolated from control and endotoxin-treated rats. Endotoxin treatment was associated with inhibition (40-50%) of gluconeogenesis from lactate plus pyruvate over a range of concentrations of substrate and of oleate and with or without glucose or glucagon. Similar inhibition was observed with asparagine, proline, glutamine, alanine and a substrate mixture, but not with glycerol, glyceraldehyde, dihydroxyacetone or endogenous substrates. There was no change in cellular ATP content or in the rates of ketogenesis or ureogenesis from asparagine, proline or glutamine. Other effects on isotopic fluxes, metabolite contents, enzyme activities and control coefficients were consistent with the suggestion that the effects of endotoxin on gluconeogenesis are exerted at the level of phosphofructokinase-1, and not at phosphoenolpyruvate carboxykinase, pyruvate kinase, pyruvate carboxylase or glucokinase.

Beta-adrenergic agonists increase amplitude of LH release in orchidectomized rats

1986 ◽  
Vol 251 (3) ◽  
pp. E316-E321
Author(s):  
S. L. Petrovic ◽  
J. C. Bedran De Castro ◽  
S. M. McCann
Keyword(s):  
Adrenergic Receptor ◽  
Receptor Agonist ◽  
Plasma Concentrations ◽  
Adrenergic Agonists ◽  
Beta Adrenergic ◽  
Releasing Hormone ◽  
The Mean ◽  
Beta 2 ◽  
Lh Releasing Hormone ◽  
Adrenergic Receptor Agonist

The role of intravenously (iv) injected adrenergic agonists in the pulsatile secretion of luteinizing hormone (LH) was examined in unanesthesized, freely behaving, castrated male rats. The alpha 2-adrenergic receptor agonist, clonidine (25 micrograms/kg), and the alpha 1-adrenergic agonist, (-)-phenylephrine (12.5 micrograms/kg), did not significantly alter pulsatile release of LH. The physiological beta 2-adrenergic receptor agonist, (-)-epinephrine (2.5 micrograms/kg), significantly increased the mean plasma concentrations of plasma LH and the amplitude of the LH pulses over a period of 70 min. The specific beta 2-receptor agonist, salmefamol, significantly increased the mean plasma concentrations of LH and especially the average amplitude of LH pulses over 70-80 min in a dose-related fashion following the injection of doses from 25 to 125 micrograms/kg. The frequency of LH pulses was not significantly increased by either agonist at any of the doses employed. Salmefamol-induced increases in plasma LH could be prevented by the beta-adrenergic blocker, bornaprolol (FM-24), in a dose-related manner. When injected together with synthetic LH-releasing hormone (400 ng/kg), salmefamol (125 micrograms/kg) significantly increased the mean plasma concentrations of LH over 70 min compared with values in controls receiving LH-releasing hormone only. The data support the concept that beta-agonists act on their receptors in the pituitary to facilitate LH-releasing hormone-induced discharge of LH.

scholarly journals Streptozotocin-induced diabetes impairs Mg2+ homeostasis and uptake in rat liver cells

2004 ◽  
Vol 286 (2) ◽  
pp. E184-E193 ◽  
Author(s):  
Theresa E. Fagan ◽  
Christie Cefaratti ◽  
Andrea Romani
Keyword(s):  
Liver Cells ◽  
Atp Content ◽  
Sprague Dawley ◽  
Uptake Mechanism ◽  
Diabetes Onset ◽  
Kinase C ◽  
Sprague Dawley Rats ◽  
Rat Liver Cells ◽  
Streptozotocin Induced Diabetes ◽  
Stimulation Of

Male Sprague-Dawley rats rendered diabetic by streptozotocin injection presented 10 and 20% decreases in total hepatic Mg2+ content at 4 and 8 wk, respectively, following diabetes onset. This decrease was associated with a parallel decrease in K+ and ATP content and an increase in Na+ level. In diabetic liver cells, the Mg2+ extrusion elicited by α1-adrenoceptor stimulation was markedly reduced compared with nondiabetic livers, whereas that induced by β-adrenoceptor stimulation was unaffected. In addition, diabetic hepatocytes did not accumulate Mg2+ following stimulation of protein kinase C pathway by vasopressin, diacylglycerol analogs, or phorbol 12-myristate 13-acetate derivates despite the reduced basal content in cellular Mg2+. Experiments performed in purified plasma membrane from diabetic livers located the defect at the level of the bidirectional Na+/Mg2+ exchanger operating in the basolateral domain of the hepatocyte cell membrane, which could extrude but not accumulate Mg2+ in exchange for Na+. The impairment of Mg2+ uptake mechanism, in addition to the decrease in cellular ATP level, can contribute to explaining the decrease in liver Mg2+ content observed under diabetic conditions.

In vitro stimulation of rat liver cells by homologous partial hepatectomy serum

In Vitro ◽  
1971 ◽  
Vol 7 (1) ◽  
pp. 1-5 ◽  
Author(s):  
Lynne P. Rutzky ◽  
William G. Taylor ◽  
Robert W. Pumper
Keyword(s):  
Partial Hepatectomy ◽  
Rat Liver ◽  
Liver Cells ◽  
Rat Liver Cells ◽  
Stimulation Of

Chronic EtOH administration alters liver Mg2+homeostasis

2003 ◽  
Vol 284 (1) ◽  
pp. G57-G67 ◽  
Author(s):  
Andrew Young ◽  
Christie Cefaratti ◽  
Andrea Romani
Keyword(s):  
Adrenergic Receptor ◽  
Prolonged Exposure ◽  
Liver Cells ◽  
Chronic Alcohol ◽  
Atp Content ◽  
Chronic Alcohol Consumption ◽  
Kinase C ◽  
And Control ◽  
Total Tissue ◽  
Stimulation Of

Ethanol (EtOH) administration to rats for 4 wk markedly decreased Mg2+ content in several tissues, including liver. Total cellular Mg2+ accounted for 26.8 ± 2.4 vs. 36.0 ± 1.4 nmol Mg2+/mg protein in hepatocytes from EtOH-fed and control rats, respectively, and paralleled a 13% decrease in cellular ATP content. Stimulation of α1- or β-adrenergic receptor or acute EtOH administration did not elicit an extrusion of Mg2+ from liver cells of EtOH-fed rats while releasing 5% of total tissue Mg2+ content from hepatocytes of control rats. Despite the 25% decrease in Mg2+ content, hepatocytes from EtOH-fed rats did not accumulate Mg2+following stimulation of protein kinase C signaling pathway, whereas control hepatocytes accumulated ∼2 nmol Mg2+ · mg protein−1 · 4 min−1. Together, these data indicate that Mg2+ homeostasis and transport are markedly impaired in liver cells after prolonged exposure to alcohol. The inability of liver cells, and possibly other tissues, to accumulate Mg2+ can help explain the reduction in tissue Mg2+ content following chronic alcohol consumption.

scholarly journals Effect of Adrenergic Agonists on High-Fat Diet-Induced Hepatic Steatosis in Mice

2020 ◽  
Vol 21 (24) ◽  
pp. 9392
Author(s):  
Yukiomi Nakade ◽  
Rena Kitano ◽  
Taeko Yamauchi ◽  
Satoshi Kimoto ◽  
Kazumasa Sakamoto ◽  
...  
Keyword(s):  
Nervous System ◽  
Hepatic Steatosis ◽  
High Fat Diet ◽  
Adrenergic Receptor ◽  
Receptor Agonist ◽  
Receptor Activation ◽  
Mrna Levels ◽  
High Fat ◽  
Adrenergic Receptor Agonist ◽  
Stimulation Of

The autonomic nervous system, consisting of sympathetic and parasympathetic branches, plays an important role in regulating metabolic homeostasis. The sympathetic nervous system (SNS) regulates hepatic lipid metabolism by regulating adrenergic receptor activation, resulting in the stimulation of hepatic very-low-density lipoprotein-triglyceride (TG) production in vivo. However, only a few studies on the relationship between SNS and hepatic steatosis have been reported. Here, we investigate the effect of adrenergic receptor agonists on hepatic steatosis in mice fed a high-fat diet (HFD). The α-adrenergic receptor agonist phenylephrine (10 mg/kg/d) or the β-adrenergic receptor agonist isoproterenol (30 mg/kg/d) was coadministered with HFD to male mice. After five weeks, hepatic steatosis, TG levels, and hepatic fat metabolism-related biomarkers were examined. HFD treatment induced hepatic steatosis, and cotreatment with phenylephrine, but not isoproterenol, attenuated this effect. Phenylephrine administration upregulated the mRNA levels of hepatic peroxisome proliferator-activated receptor alpha and its target genes (such as carnitine palmitoyltransferase 1) and increased hepatic β-hydroxybutyrate levels. Additionally, phenylephrine treatment increased the expression of the autophagosomal marker LC3-II but decreased that of p62, which is selectively degraded during autophagy. These results indicate that phenylephrine inhibits hepatic steatosis through stimulation of β-oxidation and autophagy in the liver.

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