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E Piña

Publications and source records attributed to E Piña.

At least 19 recordsLinked to original sources
PubMed2002

Non-steroidal anti-inflammatory drugs inhibit epinephrine- and cAMP-mediated lipolysis in isolated rat adipocytes.

Acute ethanol intoxication increased triacylglycerides (TAG) and thiobarbituric acid reactive substances (TBARS) in liver and promoted the liberation of epinephrine. Four non-steroidal anti-inflammatory drugs (NSAIDs)--aspirin, naproxen, nimesulide and piroxicam--prevented this increase in TAG and TBARS. Because fatty acids provided by adipose tissue contribute substantially to elevated hepatic TAG in ethanol-intoxicated rats, it was thought that the NSAIDs might reduce epinephrine-stimulated lipolysis in these rats. Isolated rat adipocytes were activated with epinephrine in the presence or absence of the NSAIDs. The NSAIDs inhibited epinephrine-stimulated lipolysis. These drugs did not modify the binding of dihydroalprenolol (beta-adrenergic agonist) to their receptors in isolated guinea-pig liver membranes. The NSAIDs, at concentrations 3,000-fold lower than that of cAMP, inhibited stimulated lipolysis by this messenger. In conclusion, aspirin, naproxen, nimesulide and piroxicam reduce the release of fatty acids from adipose tissue to the liver by inhibiting the epinephrine-stimulated lipolysis, and this, in part, explains the protective action of these NSAIDs against hepatic signs of acute ethanol intoxication.

Adipocytes↗
PubMed1999

Antagonism between the metabolic responses induced by epinephrine and piroxicam on isolated rat hepatocytes.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are one of the most employed therapeutic agents. They have a wide spectrum of biological effects, some of which are independent of cyclooxygenase inhibition, such as the alterations on the components of signal transduction systems. In particular, previous data from our laboratory suggested an antagonism between epinephrine and piroxicam, one of the most prescribed NSAIDs. Thus, this study deals with the epinephrine-piroxicam antagonism recorded for metabolic responses in isolated rat hepatocytes. The obtained results show that epinephrine stimulates lactate and ethanol consumption, stimulates glucose release from lactate only, and has no effect on cellular triacylglycerides content. Otherwise, in a dose-dependent basis, piroxicam stimulates lactate and ethanol consumption accompanied by an increase in triacylglycerides content, without changes in glucose release by hepatocytes. Piroxicam blocks the epinephrine-induced stimulation of glucose release from lactate, and epinephrine blocks the piroxicam-mediated increase in triacylglycerides content from lactate or ethanol. In contrast, the effects of epinephrine and piroxicam, promoting the consumption of lactate and ethanol, are not antagonized or added after the simultaneous administration of both compounds. This last result is probably related to the ability of both compounds to stimulate oxygen consumption. On isolated rat liver mitochondria, micromolar doses of piroxicam partially uncouple oxidative phosphorylation, and paradoxically stimulates an ATP-dependent mitochondrial function as citrullinogenesis. These results show for first time, on isolated rat hepatocytes, an antagonism between the metabolic responses of epinephrine and piroxicam, at the concentration found in plasma after its therapeutical administration.

Adenosine Diphosphate↗
PubMed1997

Ca2+ dependence of the response of three adenosine type receptors in rat hepatocytes.

The effect of three different receptor-specific adenosine agonists on the rate of ureagenesis by isolated rat hepatocytes and the dependence on the external free Ca2+ concentration ([Ca2+]e) were investigated. In the presence of high [Ca2+]e all adenosine receptor agonists increased ureagenesis to similar levels. However, with low [Ca2+]e the effects of each agonist varied as follows: (i) the adenosine A1 receptor agonist, 2-chloro-N6-cyclopentyl-adenosine, increased ureagenesis depending partially on [Ca2+]e, (ii) the adenosine receptor A2 agonist, 2-p-(-2-carboxy-ethyl) phenethylamino-5'-N-ethylcarboxyamido adenosine hydrochloride, increased ureagenesis independently of [Ca2+]e and (iii) in contrast, the adenosine receptor A3 agonist N6-2-(-4-aminophenyl) ethyladenosine, increased ureagenesis only in the presence of high [Ca2+]e. The adenosine receptor A1 antagonist, 1-allyl-3,7-dimethyl-8-phenyl xanthine, inhibited the effect of the adenosine receptor A1 agonist on ureagenesis, but not the effect of the adenosine A2 or A3 receptor agonists. The adenosine A2 receptor antagonist, 3,7-dimethyl-1-propargylxanthine, inhibited only the effect of the adenosine A2 receptor agonist. Thus, in addition to A1 and A2 type adenosine receptors, rat hepatocytes possess an A3-like adenosine receptor which responds to the addition of an adenosine A3 agonist by accelerating ureagenesis a [Ca2+]e dependent manner. Moreover, it was observed that in the presence of extracellular Ca2+ each agonist increased [Ca2+]i and this effect was inhibited by the appropriate specific antagonist.

Animals↗
PubMed1996

Piroxicam modifies the effects of ethanol on isolated rat hepatocytes.

It has been reported that piroxicam prevents the hepatic increase of triacylglycerides and thiobarbituric acid-reactive substances observed after acute ethanol intoxication in rats and also causes a decrease in blood ethanol concentration. The aim of this study was to assess the effect of piroxicam on these 3 metabolic indicators, using isolated rat hepatocytes incubated with ethanol or lactate, supplemented or not with epinephrine. Epinephrine stimulated the consumption of lactate, but not of ethanol. In the isolated hepatocytes, and in a dose-dependent fashion, piroxicam alone raised the consumption of lactate and ethanol, increased the triacylglyceride pool in cells incubated with lactate or ethanol, and decreased the content of thiobarbituric acid-reactive substances in cells incubated with ethanol, but not with lactate. Epinephrine blocked these actions of piroxicam, except the lowering of the content of thiobarbituric acid-reactive substances. Thus, piroxicam helps to control the oxidative stress produced in isolated hepatocytes by ethanol.

Animals↗
PubMed1996

Hepatic and cardiac oxidative stress and other metabolic changes in broilers with the ascites syndrome.

The objective of this study was to evaluate the gluconeogenic response of in vitro stimulated hepatocytes from control broilers and broilers with clinical manifestations of the ascites syndrome. The basal rate of glucose synthesis from lactate was found to be threefold greater in sick birds than in the control group and stimulation obtained with epinephrine was found to be quantitatively similar in both groups. Under basal conditions, the hepatocytes from the sick broilers exhibited 60% more ammonium than the control birds. In addition, the quantification of thiobarbituric acid reactive substances, as indicators of cellular lipoperoxidation, showed an increase of over 100% in heart and liver of sick broilers fowl. In conclusion, the complex integrated response of gluconeogenesis to epinephrine is maintained in broilers with ascites, although their hepatocytes present changes compatible with those observed in cases of oxidative stress. It is not known whether this stress is a cause or a consequence of the ascites syndrome.

Adenosine↗
PubMed1995

Cross-talk between glucagon- and adenosine-mediated signalling systems in rat hepatocytes: effects on cyclic AMP-phosphodiesterase activity.

The effect of adenosine analogues on glucagon-stimulated cyclic AMP accumulation in rat hepatocytes was explored. N6-Cyclopentyladenosine (CPA), 5'-N-ethylcarboxamidoadenosine and N6-(R-phenylisopropyl)adenosine inhibited in a dose-dependent manner the cyclic AMP accumulation induced by glucagon. This effect seems to be mediated through A1 adenosine receptors. Pertussis toxin completely abolished the effect of CPA on glucagon-stimulated cyclic AMP accumulation in whole cells which suggested that a pertussis-toxin-sensitive G-protein was involved. On the other hand, this action of adenosine analogues on glucagon-induced cyclic AMP accumulation was reverted by the selective low-Km cyclic AMP-phosphodiesterase inhibitor Ro 20-1724. Analysis of cyclic AMP-phosphodiesterase activity in purified hepatocyte plasma membranes showed that glucagon in the presence of GTP inhibited basal PDE activity by 45% and that CPA reverted this inhibition in dose-dependent manner. In membranes derived from pertussis-toxin-treated rats, we observed no inhibition of cyclic AMP-phosphodiesterase activity by glucagon in the absence or presence of CPA. Our results indicate that in hepatocyte plasma membranes, stimulation of adenylate cyclase activity and inhibition of a low-Km cyclic AMP phosphodiesterase activity are co-ordinately regulated by glucagon, and that A1 adenosine receptors can inhibit glucagon-stimulated cyclic AMP accumulation by blocking glucagon's effect on phosphodiesterase activity.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1994

Restoration by piroxicam of liver glutathione levels decreased by acute ethanol intoxication.

The effect of piroxicam, a nonsteroidal anti-inflammatory drug, on blood ethanol and on triacylglycerols, malondialdehyde and glutathione levels in liver of fed rats acutely intoxicated with ethanol was studied. As previously reported for fasted rats, piroxicam in fed rats decreases the concentration of ethanol in blood and inhibits the hepatic increase of triacylglycerols and malondialdehyde consequent to ethanol administration. In addition, the hepatic depletion of reduced and reduced plus oxidized glutathione observed 8 and 12h after gavage of ethanol was reversed when piroxicam was administered simultaneously with ethanol. The importance of the finding is discussed in light of the paramount participation of glutathione during the cellular oxidative stress.

Alcoholic Intoxication↗
PubMed1993

Inhibition of adenosine mediated responses in isolated hepatocytes by depolarizing concentrations of K+.

Isolated rat hepatocytes, incubated in a high K+ medium which depolarizes their plasma membrane, were used to investigate the response to adenosine. High K+ concentration blocked both the adenosine mediated increase of calcium influx and the increase in the rate of urea synthesis. It is concluded that a) adenosine stimulates calcium influx in hepatocytes probably through receptor-operated Ca2+ channels which are closed by depolarization of the plasma membrane, b) the higher cytosolic calcium concentration triggers a regulatory step that fully stimulates the rate in urea synthesis.

Adenosine↗
PubMed1993

Adenosine effect on lactate and pyruvate production in the hypoxic guinea pig heart.

1. It has been shown that adenosine stimulates glycolysis in some cells and this ability of adenosine was tested in the hypoxic guinea pig heart. 2. Adenosine (10 microM) activated lactate production in the isolated perfused guinea pig heart under conditions of normoxia but did not under hypoxia. 3. Despite this, the nucleoside favorably influenced the energy metabolism of the hypoxic heart as revealed by the better posthypoxic functional recovery (98%) compared to the control without adenosine (78%). 4. Our findings suggest a role for the glycolytic pathway in this effect of the nucleoside as long as other cardiac energy-yielding pathways are strictly aerobic.

Adenosine↗
PubMed1993

Nonsteroidal antiinflammatory drugs lower ethanol-mediated liver increase in lipids and thiobarbituric acid reactive substances.

Four nonsteroidal antiinflammatory drugs--namely, acetylsalicylic acid, naproxen, nimesulide, and dipyrone--were assayed to search their capability in preventing the hepatic increase of triacylglycerols and thiobarbituric acid reactive substances, as an indication of lipid peroxidation, resulting from the acute intoxication of rats with ethanol. The four antiinflammatory compounds inhibited the ethanol-mediated increase in triacylglycerols and thiobarbituric acid reactive substances. Furthermore, each one of these antiinflammatory drugs produced distinctive actions on blood ethanol levels: a temporal diminution with aspirin and naproxen, no changes with nimesulide, and an increase with dipyrone. It is concluded that the nonsteroidal antiinflammatory drugs contributed to controlling hepatic lipid peroxidation, and hence the oxidative stress promoted by ethanol intoxication.

Alcoholic Intoxication↗
PubMed1993

Acute ethanol intake produces lipid peroxidation in rat red blood cells membranes.

The effect of acute ethanol intake on lipid peroxidation (LP) and proteins in red blood cells (RBC) was explored. The amount of malondialdehyde (MDA; an indicator of LP) was elevated transiently when the maximal ethanol level in whole blood was observed. In contrast, erythrocyte membrane proteins were not affected. In in vitro experiments both ethanol and acetaldehyde did not alter the MDA levels. These results indicate that the metabolism of ethanol or acetaldehyde beyond the RBCs is required in order to detect LP on these cells.

Acetaldehyde↗
PubMed1992

Biochemical ethanol effects affected by a non-steroidal anti-inflammatory drug.

The non-steroidal anti-inflammatory drug, piroxicam, prevents the hepatic increase of triacylglycerols and malondialdehyde resulting from the acute intoxication of rats with ethanol. In addition, in the intoxicated rats, piroxicam consistently produces a decrease in the levels of blood ethanol in comparison with control animals. It is suggested that the anti-inflammatory compound stimulates ethanol oxidation.

Animals↗
PubMed1992

Activating effect of adenosine on rat erythrocyte glycolysis.

1. Adenosine increases the adenine nucleotide pool in rat erythrocytes. Hence, we tested the effect of the nucleoside on the glycolytic pathway in red blood cells. 2. A 2.5-fold increase in the level of fructose-1,6-bisphosphate and a 34% augmentation in lactate pool were observed in rat erythrocytes, 30 min after adenosine treatment. 3. Under conditions preventing adenosine metabolism, 1 microM nucleoside addition to isolated erythrocytes induced an 89% increase in lactate production and an increase in glucose consumption. 4. Activation of red cell phosphofructokinase (PFK) is produced by addition of microM concentrations of adenosine. Our data suggest a role for adenosine in the glycolysis flux regulation through PFK activation.

Adenosine↗
PubMed1991

Metabolic responses of isolated hepatocytes to adenosine; dependence on external calcium.

The role of cyclic-adenosine monophosphate (cAMP) and calcium (Ca2+) in the metabolic responses to adenosine was studied in isolated hepatocytes from fed rats. In the presence of 1.2 mM Ca but not in the absence of Ca2+, adenosine stimulated ureagenesis without increasing cAMP. Adenosine inhibited the glucagon mediated increase in cAMP. Adenosine increased free cytoplasmic Ca2+ provided that cells were incubated in the presence of external Ca2+. In the absence of added Ca2+ adenosine did not stimulate ureagenesis or the movements of Ca2+. It is suggested that, in the liver cell, Ca2+ may be a second messenger for adenosine.

Adenosine↗
PubMed1991

A simple method to fix and extract ATP from rat liver samples.

A simple one-step method to fix and extract ATP from rat liver samples is described. The results show that this method is suitable for fixation and extraction of the hepatic ATP content, whereas its simplicity leads to consider it the procedure of choice.

Adenosine Triphosphate↗