scholarly journals Stimulation of release of prostaglandin D2 and thromboxane B2 from perfused rat liver by extracellular adenosine

1990 ◽  
Vol 270 (1) ◽  
pp. 39-44 ◽  
Author(s):  
S vom Dahl ◽  
M Wettstein ◽  
W Gerok ◽  
D Häussinger
Keyword(s):  
Rat Liver ◽  
Portal Pressure ◽  
Thromboxane B2 ◽  
Adenosine Infusion ◽  
Isolated Perfused Rat Liver ◽  
Signal Molecules ◽  
Prostaglandin D2 ◽  
Perfused Rat Liver ◽  
Glucose Output ◽  
Stimulation Of

In isolated perfused rat liver, adenosine infusion (50 microM) led to increases in glucose output and portal pressure and a net K+ release of 3.7 +/- 0.21 mumol/g, which was followed by an equivalent net K+ uptake after cessation of the nucleoside infusion. These effects were accompanied by a transient stimulation of hepatic prostaglandin D2 and thromboxane B2 release. The Ca2+ release observed upon adenosine infusion (50 microM) was 23.5 +/- 5.2 nmol/g, i.e. 10-20% of the Ca2+ release observed with extracellular ATP (50 microM). Indomethacin (10 microM) prevented the adenosine-induced stimulation of glucose output and the increase in portal pressure by 79 and 63% respectively, and completely abolished the stimulation of prostaglandin D2 release. The thromboxane A2 receptor antagonist BM 13.177 (20 microM), the phospholipase A2 inhibitor 4-bromophenacyl bromide (20 microM) and the cyclo-oxygenase inhibitor ibuprofen (50 microM) also decreased the glycogenolytic and vasoconstrictive responses of the perfused rat liver upon adenosine infusion by 50-80%. When the indomethacin inhibition of adenosine-induced prostaglandin D2 release was titrated, a close correlation between prostaglandin D2 release and the metabolic and vascular responses to adenosine was observed. These findings suggest an important role for eicosanoids in mediating the nucleoside responses in the perfused rat liver. Since eicosanoids are known to be formed by non-parenchymal cells in rat liver [Decker (1985) Semin. Liver Dis. 5, 175-190], the present study gives further evidence for an important role of eicosanoids as signal molecules between the different liver cell populations.

scholarly journals Melittin stimulates liver glycogenolysis and the release of prostaglandin D2 and thromboxane B2

1990 ◽  
Vol 269 (1) ◽  
pp. 273-275 ◽  
Author(s):  
J A García-Sáinz ◽  
S M T Hernández-Sotomayor ◽  
M Macías-Silva
Keyword(s):  
Rat Liver ◽  
Thromboxane B2 ◽  
Prostaglandin D2 ◽  
Perfused Rat Liver ◽  
Initial Burst ◽  
Glucose Output ◽  
Liver Glycogenolysis ◽  
Stimulation Of

Melittin stimulates glycogenolysis and induces vasoconstriction in perfused rat liver. The effect was rapid and associated with production and release of prostaglandin D2 and thromboxane B2. Indomethacin blocked the release of these eicosanoids and the stimulation of glycogenolysis induced by melittin. Ibuprofen blocked the release of prostaglandin D2 induced by melittin and markedly attenuated that of thromboxane B2. Interestingly, the initial burst of glucose output induced by melittin was not inhibited by ibuprofen, although the duration of the glycogenolytic action of the peptide was greatly diminished.

Vanadate inhibits glucose output from isolated perfused rat liver

Hepatology ◽  
1991 ◽  
Vol 14 (3) ◽  
pp. 540-544 ◽  
Author(s):  
Rafael Bruck ◽  
Haia Prigozin ◽  
Zipora Krepel ◽  
Paul Rotenberg ◽  
Yoram Shechter ◽  
...  
Keyword(s):  
Rat Liver ◽  
Isolated Perfused Rat Liver ◽  
Perfused Rat Liver ◽  
Glucose Output

Endothelin-1 stimulates bile acid secretion and vesicular transport in the isolated perfused rat liver

1994 ◽  
Vol 266 (2) ◽  
pp. G324-G329 ◽  
Author(s):  
A. Tanaka ◽  
K. Katagiri ◽  
M. Hoshino ◽  
T. Hayakawa ◽  
K. Tsukada ◽  
...  
Keyword(s):  
Bile Acid ◽  
Rat Liver ◽  
Bile Flow ◽  
Low Dose ◽  
Portal Pressure ◽  
Vesicular Transport ◽  
Bile Secretion ◽  
Isolated Perfused Rat Liver ◽  
High Dose ◽  
Perfused Rat Liver

The effects of endothelin (ET) on portal pressure and bile secretion were examined using isolated perfused rat liver and rat hepatocyte preparations. ET-1 raised portal pressure dose dependently; administration at a high dose (10(-9) mol) induced a > 200% increase along with reduced bile flow and decreased secretion of bile acid and phospholipids. However, a low dose (10(-10) mol) of ET-1 brought about a < 100% portal pressure rise, enhanced both bile flow and excretion of bile acid and phospholipids, and significantly increased transfer of preadministered horseradish peroxidase (HRP) into bile. In addition, values for Ca2+ concentrations, examined by indo 1 fluorescence, were elevated in isolated hepatocytes after administration of ET-1. Papaverine suppressed the low-dose ET-1 stimulation effects on both portal pressure and bile secretion. Moreover, it also reduced the HRP excretion and suppressed intracellular Ca2+ release. This study demonstrated that ET-1 stimulates vesicular transport, probably via promotion of intracellular Ca2+ release, and, as a result, increases bile acid-dependent bile flow.

scholarly journals Metabolism of ornithine, α-ketoglutarate and arginine in isolated perfused rat liver

1995 ◽  
Vol 73 (2) ◽  
pp. 227-239 ◽  
Author(s):  
Jean Pascal De Bandt ◽  
Luc Cynober ◽  
Soo Kyung Lim ◽  
Colette Coudray-Lucas ◽  
Raoul Poupon ◽  
...  
Keyword(s):  
Rat Liver ◽  
Hepatic Metabolism ◽  
Isolated Perfused Rat Liver ◽  
Trauma Patients ◽  
Perfused Rat Liver ◽  
Metabolic Interaction ◽  
Urea Production ◽  
Stimulation Of

Ornithine (Orn; α-ketoglutarate (αKG) salt) and arginine (Arg) supplementation of enteral diets has been advocated in the treatment of hypercatabolism of trauma patients, but both compounds are subject to extensive hepatic metabolism. To compare the metabolism of these two compounds and to evaluate the possible influence of the αKG moiety, livers were perfused with αKG, Orn, ornithine α-ketoglutarate (OKG) or Arg (n 6 in each group) for 1 h. Arg uptake was nearly fourfold higher than Orn uptake (690 (SD 162) ν. 178 (SD 30) nmol/min per g liver), and Orn uptake was not modified by αKG. Orn was totally metabolized by the liver, whereas Arg led to Orn release (408 (SD 159) nmol/min per g liver) and a threefold stimulation of urea production (Arg 1·44 (SD 0·22) ν. Orn 0·45 (SD 0.09) μol/min per g liver). αKG alone only increased hepatic aspartate uptake but, when associated with Orn as OKG, it led to an increase in giutamate release and in proiine content in the liver and to a decrease in proiine uptake. From these findings we conclude that (1) Arg load is extensively metabolized by the liver, inducing urea production, (2) in enteral use, Orn supplementation appears preferable to Arg as it is less ureogenic (as also recently demonstrated in vivo in stressed rats receiving isomolar amounts of Arg and Orn), (3) the liver participates in the Orn-αKG metabolic interaction, mostly in proiine metabolism, which occurs in the splanchnic area.

scholarly journals Effect of phenylephrine on glutamate and glutamine metabolism in isolated perfused rat liver

1984 ◽  
Vol 221 (3) ◽  
pp. 651-658 ◽  
Author(s):  
D Häussinger ◽  
H Sies
Keyword(s):  
Glutamate Dehydrogenase ◽  
Rat Liver ◽  
Glutamine Metabolism ◽  
Isolated Perfused Rat Liver ◽  
Perfused Rat Liver ◽  
Alpha Adrenergic Receptors ◽  
14Co2 Production ◽  
Oxoglutarate Dehydrogenase ◽  
Glutamine Uptake ◽  
Stimulation Of

Addition of phenylephrine to isolated perfused rat liver is followed by an increased 14CO2 production from [1-14C]glutamate, [1-14C]glutamine, [U-14C]proline and [3-14C]pyruvate, but by a decreased 14CO2 production from [1-14C]pyruvate. Simultaneously, there is a considerable decrease in tissue content of 2-oxoglutarate, glutamate and citrate. Stimulation of 14CO2 production from [1-14C]glutamate is also observed in the presence of amino-oxyacetate, suggesting a stimulation of glutamate dehydrogenase and 2-oxoglutarate dehydrogenase fluxes by phenylephrine. Inhibition of pyruvate dehydrogenase flux by phenylephrine is due to an increased 2-oxoglutarate dehydroxygenase flux. Phenylephrine stimulates glutaminase flux and inhibits glutamine synthetase flux to a similar extent, resulting in an increased hepatic glutamine uptake. Whereas the effects of NH4+ ions and phenylephrine on glutaminase flux were additive, activation of glutaminase by glucagon was considerably diminished in the presence of phenylephrine. The reported effects are largely overcome by prazosin, indicating the involvement of alpha-adrenergic receptors in the action of phenylephrine. It is concluded that stimulation of gluconeogenesis from various amino acids by phenylephrine is due to an increased flux through glutamate dehydrogenase and the citric acid cycle.

scholarly journals Prostaglandin F2α and the thromboxane A2 analogue ONO-11113 stimulate Ca2+ fluxes and other physiological responses in rat liver. Further evidence that prostanoids may be involved in the action of arachidonic acid and platelet-activating factor

1988 ◽  
Vol 249 (3) ◽  
pp. 677-685 ◽  
Author(s):  
J G Altin ◽  
F L Bygrave
Keyword(s):  
Arachidonic Acid ◽  
Portal Pressure ◽  
Platelet Activating Factor ◽  
Prostaglandin F2α ◽  
Thromboxane A2 ◽  
Prostaglandin D2 ◽  
O2 Uptake ◽  
Glucose Output ◽  
Thromboxane A2 Analogue ◽  
Stimulation Of

The administration of prostaglandin F2 alpha (PGF2 alpha) and the thromboxane A2 analogue, ONO-11113, to rat livers perfused with media containing either 1.3 mM- or 10 microM-Ca2+ was followed by a stimulation of Ca2+ efflux, changes in O2 uptake and glucose output, and increase in portal pressure. The responses elicited by 5 microM-PGF2 alpha were similar to those induced by the alpha-adrenergic agonist phenylephrine. At both 1.3 mM and 10 microM extracellular Ca2+, PGF2 alpha induced Ca2+ efflux (70-90 nmol/g of liver), probably from the same source as that released by phenylephrine. Prostaglandin D2 (5 microM) and prostaglandin E2 (5 microM) also induced responses, but these were generally much smaller (less than 30%) than those induced by PGF2 alpha. Similarly to vasopressin and other Ca2+-mobilizing hormones, PGF2 alpha also interacted synergistically with glucagon (and cyclic AMP) in stimulating Ca2+ influx both in the perfused liver and in isolated hepatocytes. By comparison with phenylephrine and PGF2 alpha, ONO-11113 was much more potent in inducing vasoconstriction, and, at concentrations of 10-200 nM, induced a different pattern of changes in Ca2+ flux, respiration and glycogenolysis. There was first a rapid efflux of Ca2+ (45-60 nmol/g of liver), followed by a smaller Ca2+ influx, and a further release of Ca2+ (approx. 90 nmol/g of liver) when ONO-11113 was removed. Respiration was first stimulated but then markedly inhibited. At concentrations less than 5 nM, ONO-11113 induced a sustained stimulation of O2 uptake and a more prolonged efflux of Ca2+, with less Ca2+ efflux occurring upon the removal of the agent. Glycogenolysis followed a pattern which was similar to the Ca2+ response. Co-administration of glucagon did not potentiate Ca2+ influx by ONO-11113, but the action of ONO-11113 was inhibited (50%) by a few minutes' prior administration of 10 nM-vasopressin. The vasoconstrictive action of ONO-11113 was synergistically potentiated by the co-administration of phenylephrine. Since the actions of arachidonic acid, platelet-activating factor and lysophosphatidylcholine in liver were recently found to be cyclo-oxygenase-sensitive, the results provide strong evidence that at least PGF2 alpha and thromboxane A2 may be involved in mediating the action of these agents.

scholarly journals The Influence of Ca2+ on Gluconeogenesis Stimulation by Glucagon in the Liver of Arthritic Rats

2002 ◽  
Vol 45 (3) ◽  
pp. 309-315 ◽  
Author(s):  
Ana M. Kelmer-Bracht ◽  
Zélio Fedatto-Júnior ◽  
Emy L. Ishii-Iwamoto ◽  
Silvana M. Caparroz-Assef ◽  
Adelar Bracht
Keyword(s):  
Rat Liver ◽  
Experimental System ◽  
Isolated Perfused Rat Liver ◽  
Perfused Rat Liver ◽  
Hepatic Gluconeogenesis ◽  
Dependent Component ◽  
Stimulation Of

Ca2+ participates in the stimulation of hepatic gluconeogenesis by glucagon and there is evidence that Ca2+ fluxes are modified in arthritic rats. These findings raise the question whether hepatic gluconeogenesis in arthritic rats responds differently to glucagon and Ca2+. The experimental system was the isolated perfused rat liver. In the presence of Ca2+, stimulation of hepatic gluconeogenesis by glucagon in arthritic rats was equal to that in normal rats in absolute terms, but higher in relative terms (104.5 and 45.2%, respectively). In the absence of Ca2+, however, stimulation of hepatic gluconeogenesis by glucagon in arthritic rats was smaller in both absolute and relative terms (18.5 and 41.9%, respectively). It can be concluded that the Ca2+-dependent component of gluconeogenesis activation by glucagon is more important in arthritic than in normal rats.

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