scholarly journals Hepatic inositol release upon hormonal stimulation of perfused rat liver

1988 ◽  
Vol 251 (3) ◽  
pp. 843-848 ◽  
Author(s):  
S vom Dahl ◽  
P Graf ◽  
H Sies
Keyword(s):  
Cyclic Amp ◽  
Rat Liver ◽  
Radioactive Material ◽  
Perfused Rat Liver ◽  
Dibutyryl Cyclic Amp ◽  
Hormonal Stimulation ◽  
Metabolic Difference ◽  
Basal Release ◽  
Stimulation Of ◽  
Sustained Increase

A sustained increase in the hepatic release of 3H radioactivity was shown to occur upon hormonal stimulation of perfused rat liver 15-20 h after intraperitoneal injection of 100 microCi of myo-[2-3H]inositol. Hormone-released radioactive material was analysed by t.l.c. and was found to consist predominantly of [3H]inositol, without further metabolites. Vasopressin (14 nM), phenylephrine (1.7 microM), angiotensin II (15 nM), glucagon (0.5 nM) and dibutyryl cyclic AMP (5 microM) exert maximal effects on hepatic inositol efflux after 10-15 min of stimulation. Omission of Ca2+ from the perfusion medium abolishes the hormone-dependent inositol release. LiCl (10 mM) does not significantly affect the basal release of [3H]inositol, but suppresses vasopressin- and angiotensin-triggered inositol release. Inositol efflux induced by glucagon, dibutyryl cyclic AMP and phenylephrine, however, remains essentially unchanged by LiCl infusion. This establishes a further metabolic difference between these two groups of agonists in that stimuli that act through cyclic AMP produce a stimulated outflow of inositol, but apparently without a Li+-sensitive phosphatase being involved in the overall process.

scholarly journals Hepatic thiol and glutathione efflux under the influence of vasopressin, phenylephrine and adrenaline

1985 ◽  
Vol 226 (2) ◽  
pp. 545-549 ◽  
Author(s):  
H Sies ◽  
P Graf
Keyword(s):  
Plasma Membrane ◽  
Cyclic Amp ◽  
Rat Liver ◽  
Isolated Perfused Rat Liver ◽  
Peripheral Inflammation ◽  
Perfused Rat Liver ◽  
Dibutyryl Cyclic Amp ◽  
Hormone Dependence ◽  
Experimental Shock ◽  
Hormone Effects

Thiol and glutathione (GSH) efflux across the sinusoidal plasma membrane in isolated perfused rat liver was stimulated by addition of hormones such as vasopressin, phenylephrine and adrenaline, whereas glucagon or dibutyryl cyclic AMP were without effect. Phenylephrine and adrenaline effects were sensitive to prazosin and phentolamine, respectively. The increase in thiol efflux was largely accounted for by an increase in GSH efflux. Thiol efflux and the hormone effects were abolished in GSH-depleted liver. Biliary GSH efflux was diminished upon hormone addition. The newly discovered hormone-dependence of GSH release across the sinusoidal plasma membrane may explain the known loss of GSH during conditions of experimental shock (traumatic or endotoxin) and stress and peripheral inflammation.

scholarly journals The cytosolic concentration of phosphate determines the maximal rate of glycogenolysis in perfused rat liver

1990 ◽  
Vol 266 (1) ◽  
pp. 207-212 ◽  
Author(s):  
F Vanstapel ◽  
M Waebens ◽  
P Van Hecke ◽  
C Decanniere ◽  
W Stalmans
Keyword(s):  
Cyclic Amp ◽  
Rat Liver ◽  
Glycogen Phosphorylase ◽  
Perfused Rat Liver ◽  
Maximal Rate ◽  
Free Medium ◽  
Progressive Decrease ◽  
Dibutyryl Cyclic Amp ◽  
Initial Value ◽  
Contrast Exposure

Glycogenolysis was studied in glycogen-rich perfused livers in which glycogen phosphorylase was fully converted into the a form by exposure of the livers to dibutyryl cyclic AMP. We monitored intracellular Pi by 31P n.m.r. Perfusion with Pi-free medium during 30 min caused a progressive decrease of the Pi signal to 50% of its initial value. In contrast, exposure of the livers to KCN and/or 2,4-dinitrophenol resulted in a rapid doubling of the Pi signal. Alterations in the intracellular Pi coincided with proportional changes in the rate of hepatic glycogenolysis (measured as the output of glucose plus lactate). The results indicate that the rate of glycogenolysis catalysed by phosphorylase a depends linearly on the hepatic Pi concentration. Hence the Km of phosphorylase a for its substrate Pi must be considerably higher than the concentrations that occur in the cytosol, even during hypoxia.

scholarly journals Sustained oscillations in extracellular calcium concentrations upon hormonal stimulation of perfused rat liver

1987 ◽  
Vol 241 (3) ◽  
pp. 933-936 ◽  
Author(s):  
P Graf ◽  
S vom Dahl ◽  
H Sies
Keyword(s):  
Angiotensin Ii ◽  
Rat Liver ◽  
Perfused Rat Liver ◽  
Hormone Concentration ◽  
Oscillatory Behaviour ◽  
Hormonal Stimulation ◽  
Isolated Rat Liver ◽  
Sustained Oscillations ◽  
Isolated Rat ◽  
Stimulation Of

Sustained oscillations in extracellular free Ca2+ were shown to occur on addition of vasopressin, phenylephrine or angiotensin II in isolated rat liver perfused with low (10 microM)-Ca2+ medium. The amplitude and frequency of oscillation depend on hormone concentration. In contrast, Ca2+ releases on addition of ATP, t-butyl hydroperoxide or arachidonate do not exhibit oscillatory behaviour. The vasopressin-induced oscillations were suppressed by glucagon and dibutyryl 3′,5′-cyclic AMP, but not by dibutyryl 3′,5′-cyclic GMP. These observations in the extracellular space complement observations by Woods, Cuthbertson & Cobbold [(1986) Nature (London) 319, 600-602] on oscillations in intracellular free Ca2+ in single liver cells.

Control of brown adipose tissue lipolysis and respiration by adenosine

1983 ◽  
Vol 245 (6) ◽  
pp. E555-E559 ◽  
Author(s):  
D. Szillat ◽  
L. J. Bukowiecki
Keyword(s):  
Adipose Tissue ◽  
Cyclic Amp ◽  
Palmitic Acid ◽  
Brown Adipose Tissue ◽  
Brown Adipocyte ◽  
Tissue Respiration ◽  
Dibutyryl Cyclic Amp ◽  
Response Curves ◽  
Brown Adipose ◽  
Stimulation Of

Adenosine competitively inhibited the stimulatory effects of (-)-isoproterenol on lipolysis and respiration in hamster brown adipocytes. The low value of the apparent ki for respiratory inhibition by adenosine (7 nM) indicated that the nucleoside may control brown adipocyte function under physiological concentrations. Significantly, the dose-response curves for isoproterenol stimulation of lipolysis and respiration were both shifted by adenosine to higher agonist concentrations by the same order of magnitude, providing additional evidence for a tight coupling between lipolysis and respiration. The inhibitory effects of adenosine were rapidly reversed by a) adenosine deaminase, b) agents known to increase intracellular cyclic AMP levels (isoproterenol, isobutylmethylxanthine, dibutyryl cyclic AMP), and c) direct stimulation of respiration with palmitic acid. These results, combined with the fact that adenosine failed to affect respiration evoked either by dibutyryl cyclic AMP or by palmitic acid, strongly indicate that adenosine regulates brown adipose tissue respiration at an early metabolic step of the stimulus-thermogenesis sequence, most probably at the level of the adenylate cyclase complex.

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