scholarly journals Determination of mitochondrial calcium content in hepatocytes by a rapid cellular-fractionation technique. α-adrenergic agonists do not mobilize mitochondrial Ca2+

1984 ◽  
Vol 219 (2) ◽  
pp. 383-389 ◽  
Author(s):  
S B Shears ◽  
C J Kirk
Keyword(s):  
Glycogen Phosphorylase ◽  
Preceding Paper ◽  
Calcium Content ◽  
Total Cell ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Energy Dependent ◽  
Glycogen Phosphorylase Activity ◽  
Alpha Adrenergic Agonist

A rapid cellular fractionation technique [the preceding paper, Shears & Kirk (1984) Biochem. J., 219, 375-382] was employed to separate a mitochondria-rich fraction from hepatocytes within seconds. Mitochondrial Ca was estimated to be no more than 41% of total cell Ca. At least half of the mitochondrial Ca was present in an energy-dependent pool; 20% of total cell Ca was accessible to EGTA within 10s. The alpha-adrenergic agonist phenylephrine stimulated glycogen phosphorylase activity by 100% within 0.5 min and induced a loss of 20% of total cell Ca after 10 min from the EGTA-inaccessible pool. However, between 0.5 and 10 min after the addition of phenylephrine to hepatocytes there was no significant change in the Ca content of the mitochondria-rich fraction. Hepatocytes that were preloaded with Ca2+ during 90 min incubation at 0-4 degrees C expelled this cation during 20 min incubation at 37 degrees C. After this time, phenylephrine failed to alter the Ca content of a mitochondria-rich fraction. It is concluded that alpha-adrenergic agonists do not mobilize Ca2+ from hepatocyte mitochondria.

scholarly journals Determination of mitochondrial calcium content in hepatocytes by a rapid cellular fractionation technique. Vasopressin stimulates mitochondrial Ca2+ uptake

1984 ◽  
Vol 220 (2) ◽  
pp. 417-421 ◽  
Author(s):  
S B Shears ◽  
C J Kirk
Keyword(s):  
Glycogen Phosphorylase ◽  
Calcium Content ◽  
Transient Increase ◽  
Mitochondrial Calcium ◽  
Phosphorylase Activity ◽  
Hormone Stimulation ◽  
Control Value ◽  
Glycogen Phosphorylase Activity ◽  
Stimulation Of

Stimulation of hepatocytes with vasopressin (10 nM) in the presence of 1.25 mM extracellular Ca2+ increased glycogen phosphorylase activity 4-fold within 15s and provoked a rapid efflux of cell-associated Ca2+. Vasopressin also caused a transient increase in the Ca content of a mitochondria-rich fraction separated within seconds of hormone stimulation by a rapid fractionation technique [Shears & Kirk (1984) Biochem. J. 219, 375-382]. The Ca content of this fraction was restored to the control value within 2 min of hormone addition. These results indicate that mitochondria are not the source of the cell-associated Ca which is mobilized in the cytosol of vasopressin-stimulated hepatocytes. Rather, these organelles buffer the increase in cytosol [Ca2+] attributable to Ca mobilization from non-mitochondrial sources.

Effect of adrenergic agonists on big and small renin

1980 ◽  
Vol 238 (5) ◽  
pp. E416-E420
Author(s):  
H. Iwao ◽  
C. S. Lin ◽  
A. M. Michelakis
Keyword(s):  
Submaxillary Gland ◽  
Plasma Renin ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
Molecular Weights ◽  
Submaxillary Glands ◽  
Beta Adrenergic Agonists ◽  
Beta Adrenergic Agonist ◽  
Alpha Adrenergic Agonist

The effect of alpha- and beta-adrenergic agonists on renal and submaxillary renin of different molecular weights was studied using male albino mice as experimental animals. Phenylephrine or isoproterenol was administered intravenously after removal of the submaxillary glands and/or kidneys. Renin was isolated from plasma by column chromatography and then measured by a direct radioimmunoassay. Phenylephrine increased both 68,500-dalton renin (big renin) and 38,000-dalton renin (small renin) in the plasma of nephrectomized mice. Isoproterenol increased big and small renin in the plasma of mice whose submaxillary glands were removed. In both cases, the increase of small renin was significantly greater than that of big renin. The results suggest that the alpha-adrenergic agonist phenylephrine affects the submaxillary gland, leading to the increase of both big and small plasma renin. In contrast, the beta-adrenergic agonist isoproterenol affects the kidney, leading to the increase of both big and small plasma renin.

Regulation of Trypanosoma cruzi infectivity by alpha- and beta-adrenergic agonists: desensitization produced by prolonged treatments or increasing agonist concentrations

Parasitology ◽  
1990 ◽  
Vol 100 (3) ◽  
pp. 429-434 ◽  
Author(s):  
A. Ayala ◽  
F. Kierszenbaum
Keyword(s):  
Trypanosoma Cruzi ◽  
Prolonged Exposure ◽  
Inhibitory Effect ◽  
Tissue Level ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
Beta Adrenergic Agonists ◽  
Alpha Adrenergic Agonist

SUMMARYWe previously reported that blood forms of Trypanosoma cruzi express alpha- and beta-adrenergic receptors and that binding of specific agonists to these receptors modifies the infective capacity of the parasite in vitro. The present study has revealed that the inhibitory effect of the beta-adrenergic agonist L-isoproterenol and the stimulatory effect of the alpha-adrenergic agonist L-phenylephrine are not produced when the parasite is subjected to prolonged exposure to otherwise effective doses of these agonists or when supraoptimal doses of these agonists are used. We refer to these phenomena as ‘desensitization’ because of their analogy with vertebrate cells becoming desensitized by prolonged exposure to, or relatively high concentrations of, adrenergic agonists. At a constant agonist concentration, T. cruzi desensitization was time-dependent and, when the time of parasite treatment with the agonists was not changed, the higher concentrations of the agonist tested were the most effective in producing desensitization. The reduced infectivity resulting from treatment with optimal doses of L-isoproterenol was accompanied by elevated levels of cyclic adenosine mono- phosphate (cAMP) which were not detectable when L-isoproterenol concentrations producing desensitization were used. This finding implicated cAMP as a likely second signal in the inhibitory mechanisms of this agonist. No significant change in cAMP was detectable in parasites treated with L-phenylephrine, leaving open the question about how optimal doses of this alpha-adrenergic agonist enhance T. cruzi infectivity. Parasite responsiveness to alpha- and beta-adrenergic agonists as well as the desensitization effects define a system which regulates infectivity and could be modified at the host tissue level by naturally occurring agonists.

Suppression of alpha adrenergic agonist-induced catalepsy in mice by potentized Agaricus muscarius

1997 ◽  
Vol 86 (03) ◽  
pp. 139-141 ◽  
Author(s):  
Souvik Ghosh ◽  
Sinha Babu ◽  
N.C. Sukul
Keyword(s):  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Swiss Albino Mice ◽  
Albino Mice ◽  
Alpha Adrenergic Agonist

Abstract Agaricus muscarius 30c, a potentized homoeopathic drug prepared by successive dilution with 90% ethanol followed by sonication in 30 steps, suppressed catalepsy induced by alpha adrenergic agonists in Swiss albino mice. Agaricus produced anticataleptic effect when it was administered orally and no such effect when administered intraperitoneally. The alpha 1 agonist phenylephrine and alpha 2 agonist clonidine were administered intraperitoneally to mice at a dose of 2 mg/kg and 1 mg/kg, respectively. Mice were pretreated orally with Agaricus muscarius 30c. The action of Agaricus is thought to be mediated through ororeceptors.

scholarly journals Stable changes to calcium fluxes in mitochondria isolated from rat livers perfused with α-adrenergic agonists and with glucagon

1980 ◽  
Vol 188 (2) ◽  
pp. 443-450 ◽  
Author(s):  
Wayne M. Taylor ◽  
Veronica Prpić ◽  
John H. Exton ◽  
Fyfe L. Bygrave
Keyword(s):  
Adenine Nucleotides ◽  
Calcium Content ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Short Term ◽  
Adrenergic Antagonist ◽  
Prolonged Retention ◽  
Nadph Oxidation ◽  
Reduced Rate ◽  
Rat Livers

Mitochondria isolated from rat liver after a short-term perfusion with the α-adrenergic agonist phenylephrine or with glucagon exhibited enhanced rates of uptake of Ca2+ and prolonged retention of Ca2+ in the presence of 4mm-Pi. The effect of Ca2+ retention was apparent after perfusion with phenylephrine for only 1min and was maximal after 7min of treatment. The changes induced by glucagon, although similar, were less rapid. Adrenaline caused similar changes to phenylephrine and its effects were blocked by the α-adrenergic antagonist phenoxybenzamine, but not by the β-antagonist propranolol. The Ca2+ content of the isolated mitochondria decreased by 30% 1min after the onset of perfusion with phenylephrine; by 6min it had begun to return to the original value which was reached at 10min. A similar loss in calcium content was induced by glucagon but the changes were not as great and occurred more slowly. Mitochondria from phenylephrine-treated livers exhibited decreased rates of Ca2+ efflux induced by addition of 2mm-EGTA, a 50% increase in the contents of ADP and total adenine nucleotides, a small increase in the transmembrane pH gradient, and a reduced rate of oxaloacetate-induced NADPH oxidation. This study thus shows that stimulation of liver by α-adrenergic agonists, like that by glucagon, induces within minutes a stable modification of mitochondria leading to alterations in the Ca2+-translocation cycle (increased Ca2+ uptake and retention) and alterations in mitochondrial energy-linked reactions.

scholarly journals The contribution of both extracellular and intracellular calcium to the action of α-adrenergic agonists in perfused rat liver

1984 ◽  
Vol 220 (1) ◽  
pp. 35-42 ◽  
Author(s):  
P H Reinhart ◽  
W M Taylor ◽  
F L Bygrave
Keyword(s):  
Rat Liver ◽  
Perfused Rat Liver ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Redox Ratio ◽  
Lactate And Pyruvate ◽  
Body Production ◽  
Sustained Responses ◽  
Alpha Adrenergic Agonist

The role of both intracellular and extracellular Ca2+ pools in the expression of alpha-adrenergic-agonist-mediated responses was examined in perfused rat liver. Responses studied included glycogenolysis, respiration, lactate and pyruvate formation, ketone-body production, changes in the cytoplasmic and mitochondrial redox ratio and cellular K+ fluxes. Each of these was shown to be dependent on the mobilization of intracellular Ca2+ and can be grouped into one of two response types. Transient responses (ion fluxes and the redox ratios) are obligatorily dependent on the mobilization of intracellular Ca2+ and occur irrespective of the extracellular Ca2+ concentration. Sustained responses, on the other hand, initially require intracellular Ca2+ and, subsequently, extracellular Ca2+. The data indicate that alpha-adrenergic agonists mobilize extracellular Ca2+ as well as intracellular Ca2+ and that both pools are required for the full expression of hormone-induced responses in rat liver.

VASCULAR CONNECTIVE TISSUE UNDER THE INFLUENCE OF THYROXINE

1961 ◽  
Vol 36 (2) ◽  
pp. 197-211 ◽  
Author(s):  
lb Lorenzen
Keyword(s):  
Connective Tissue ◽  
Vessel Wall ◽  
Aortic Wall ◽  
Calcium Content ◽  
Sodium Sulphate ◽  
Collagen Content ◽  
Histological Changes ◽  
Hexosamine Content ◽  
Healing Processes

ABSTRACT Biochemical and histological changes in the aortic wall of rabbits were demonstrated following injection of epinephrine and l-thyroxine during 2 weeks. The widespread gross and microscopic changes were accompanied by an increase in hexosamine content and uptake of 35S labeled sodium sulphate, and an increased calcium content, whereas the collagen content, assessed by determination of hydroxyproline, was reduced. Comparison with the effect of epinephrine injections alone showed that thyroxine intensified the damaging effect of epinephrine on the vessel wall and induced more pronounced mucopolysaccharide changes in the aortic wall, presumably acting as a link in the healing processes.

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