scholarly journals The effects of alpha-adrenergic agonists on the regulation of the branched chain alpha-ketoacid oxidation in the perfused rat liver.

1982 ◽  
Vol 257 (23) ◽  
pp. 14318-14323
Author(s):  
D Buxton ◽  
L L Barron ◽  
M S Olson
Keyword(s):  
Rat Liver ◽  
Perfused Rat Liver ◽  
Adrenergic Agonists ◽  
Branched Chain

scholarly journals The action of α-adrenergic agonists on plasma-membrane calcium fluxes in perfused rat liver

1984 ◽  
Vol 220 (1) ◽  
pp. 43-50 ◽  
Author(s):  
P H Reinhart ◽  
W M Taylor ◽  
F L Bygrave
Keyword(s):  
Plasma Membrane ◽  
Rat Liver ◽  
Potential Role ◽  
Dependent Manner ◽  
Perfused Rat Liver ◽  
Adrenergic Agonists ◽  
Mediated Effects ◽  
Alpha Agonist ◽  
Alpha Adrenergic Agonist

The effect of alpha-adrenergic agonists on Ca2+ fluxes was examined in the perfused rat liver by using a combination of Ca2+-electrode and 45Ca2+-uptake techniques. We showed that net Ca2+ fluxes can be described by the activities of separate Ca2+-uptake and Ca2+-efflux components, and that alpha-adrenergic agonists modulate the activity of both components in a time-dependent manner. Under resting conditions, Ca2+-uptake and -efflux activities are balanced, resulting in Ca2+ cycling across the plasma membrane. The alpha-adrenergic agonists vasopressin and angiotensin, but not glucagon, stimulate the rate of both Ca2+ efflux and Ca2+ uptake. During the first 2-3 min of alpha-agonist administration the effect on the efflux component is the greater, the net effect being efflux of Ca2+ from the cell. After 3-4 min of phenylephrine treatment, net Ca2+ movements are essentially complete, however, the rate of Ca2+ cycling is significantly increased. After removal of the alpha-agonist a large stimulation of the rate of Ca2+ uptake leads to the net accumulation of Ca2+ by the cell. The potential role of these Ca2+ flux changes in the expression of alpha-adrenergic-agonist-mediated effects is discussed.

scholarly journals The Ca2+-mobilizing actions of vasopressin and angiotensin differ from those of the α-adrenergic agonist phenylephrine in the perfused rat liver

1985 ◽  
Vol 232 (3) ◽  
pp. 911-917 ◽  
Author(s):  
J G Altin ◽  
F L Bygrave
Keyword(s):  
Plasma Membrane ◽  
Rat Liver ◽  
Similar Amount ◽  
Perfused Rat Liver ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Hormone Administration ◽  
Sensitive Electrode ◽  
Stimulation Of

A Ca2+-sensitive electrode was used to study net Ca2+-flux changes induced by the administration of phenylephrine, vasopressin and angiotensin to the perfused rat liver. The studies reveal that, although the Ca2+ responses induced by vasopressin and angiotensin are similar, they are quite different from the Ca2+ fluxes induced by phenylephrine. The administration of phenylephrine is accompanied by a stimulation of a net amount of Ca2+ efflux (140 nmol/g of liver). A re-uptake of a similar amount of Ca2+ occurs only after the hormone is removed. In contrast, the administration of vasopressin or angiotensin to livers perfused with 1.3 mM-Ca2+ induces the release of a relatively small amount of Ca2+ (approx. 40 nmol/g of liver) during the first 60 s. This is followed by a much larger amount of Ca2+ uptake (70-140 nmol/g of liver) after 1-2.5 min of hormone administration, and a slow efflux or loss of a similar amount of Ca2+ over a period of 6-8 min. At lower concentrations of perfusate Ca2+ (less than 600 microM) these hormones induce only a net efflux of the ion. These results suggest that at physiological concentrations of extracellular Ca2+ the mechanism by which alpha-adrenergic agonists mobilize cellular Ca2+ is different from that involving vasopressin and angiotensin. It seems that the hormones may have quite diverse effects on Ca2+ transport across the plasma membrane and perhaps organellar membranes in liver.

scholarly journals Stimulation by α-adrenergic agonists of Ca2+ fluxes, mitochondrial oxidation and gluconeogenesis in perfused rat liver

1983 ◽  
Vol 212 (3) ◽  
pp. 555-565 ◽  
Author(s):  
W M Taylor ◽  
P H Reinhart ◽  
F L Bygrave
Keyword(s):  
Rat Liver ◽  
Tricarboxylic Acid Cycle ◽  
Acid Oxidation ◽  
Perfused Rat Liver ◽  
Adrenergic Agonists ◽  
Mitochondrial Oxidation ◽  
Phenylephrine Infusion ◽  
Glucose Output ◽  
Beta Hydroxybutyrate ◽  
Adrenergic Activation

Glucose output from perfused livers of 48 h-starved rats was stimulated by phenylephrine (2 microM) when lactate, pyruvate, alanine, glycerol, sorbitol, dihydroxyacetone or fructose were used as gluconeogenic precursors. Phenylephrine-induced increases in glucose output were immediately preceded by a transient efflux of Ca2+ and a sustained increase in oxygen uptake. Phenylephrine decreased the perfusate [lactate]/[pyruvate] ratio when sorbitol or glycerol was present, but increased the ratio when alanine, dihydroxyacetone or fructose was present. Phenylephrine induced a rapid increase in the perfusate [beta-hydroxybutyrate]/[acetoacetate] ratio and increased total ketone-body output by 40-50% with all substrates. The oxidation of [1-14C]octanoate or 2-oxo[1-14C]glutarate to 14CO2 was increased by up to 200% by phenylephrine. All responses to phenylephrine infusion were diminished after depletion of the hepatic alpha-agonist-sensitive pool of Ca2+ and returned toward maximal responses after Ca2+ re-addition. Phenylephrine-induced increases in glucose output from lactate, sorbitol and glycerol were inhibited by the transaminase inhibitor amino-oxyacetate by 95%, 75% and 66% respectively. Data presented suggest that the mobilization of an intracellular pool of Ca2+ is involved in the activation of gluconeogenesis by alpha-adrenergic agonists in perfused rat liver. alpha-Adrenergic activation of gluconeogenesis is apparently accompanied by increases in fatty acid oxidation and tricarboxylic acid-cycle flux. An enhanced transfer of reducing equivalents from the cytoplasmic to the mitochondrial compartment may also be involved in the stimulation of glucose output from the relatively reduced substrates glycerol and sorbitol and may arise principally from an increased flux through the malate-aspartate shuttle.

scholarly journals The stimulation of tricarboxylic acid-cycle flux by α-adrenergic agonists in perfused rat liver

1986 ◽  
Vol 233 (2) ◽  
pp. 321-324 ◽  
Author(s):  
W M Taylor ◽  
E van de Pol ◽  
F L Bygrave
Keyword(s):  
Rat Liver ◽  
Tricarboxylic Acid Cycle ◽  
Tricarboxylic Acid ◽  
Perfused Rat Liver ◽  
Adrenergic Agonists ◽  
Acid Cycle ◽  
Total Tissue ◽  
Stimulation Of

Output of 14CO2 from 1-14C-labelled glutamate, 2-oxoglutarate or octanoate and from 4-methyl-2-oxo[2-14C]pentanoate was increased by more than 100% after infusion of phenylephrine into perfused livers of fed rats. Infusion of ethanol or sorbitol raised 3-hydroxybutyrate/acetoacetate ratios and decreased the output of 14CO2. Increases in 14CO2 output induced by phenylephrine were observed in the presence or absence of ethanol or sorbitol and were accompanied by elevated 3-hydroxybutyrate/acetoacetate ratios under all conditions examined. Phenylephrine had no effect on total tissue ATP/ADP ratios in livers from fed or starved rats. The data suggest that phenylephrine-induced increases in tricarboxylic acid-cycle flux do not arise from lowered matrix NADH/NAD+ or ATP/ADP ratios.

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