scholarly journals α1-Adrenergic stimulation of Ca2+ mobilization without phosphorylase activation in hepatocytes from phosphorylase b kinase-deficient gsd/gsd rats

1981 ◽  
Vol 198 (2) ◽  
pp. 379-383 ◽  
Author(s):  
P F Blackmore ◽  
J H Exton
Keyword(s):  
Strong Evidence ◽  
Liver Cells ◽  
Ionophore A23187 ◽  
Adrenergic Stimulation ◽  
Bivalent Cation ◽  
Site Of Action ◽  
Adrenergic Activation ◽  
Stimulation Of

Phenylephrine, vasopressin and the bivalent cation ionophore A23187 mobilized Ca2+ normally, but failed to activate phosphorylase, in hepatocytes from gsd/gsd rats with a deficiency of liver phosphorylase b kinase. These data provide strong evidence that phosphorylase b kinase is the site of action of the Ca2+ mobilized intracellularly during alpha 1-adrenergic activation of phosphorylase in liver cells.

scholarly journals Relationship between hormonal activation of phosphatidylinositol hydrolysis, fluid secretion and calcium flux in the blowfly salivary gland

1979 ◽  
Vol 178 (1) ◽  
pp. 45-58 ◽  
Author(s):  
J N Fain ◽  
M J Berridge
Keyword(s):  
Salivary Gland ◽  
Fluid Secretion ◽  
Salivary Secretion ◽  
Calcium Flux ◽  
Ionophore A23187 ◽  
Bivalent Cation ◽  
Inositol 1 ◽  
Low Concentrations ◽  
Hormonal Activation ◽  
Stimulation Of

The addition of 5-hydroxytryptamine to the isolated blowfly salivary gland stimulates fluid secretion, transepithelial calcium transport and the breakdown of 32P- or 3H-labelled phosphatidylinositol The breakdown of [32P]phosphatidylcholine and [32P]-phosphatidylethanolamine was not stimulated by 5-hydroxytryptamine. In salivary glands incubated with myo-[2-3H]inositol for 1–3 h, more than 95% of the label retained by the tissue was in the form of phosphatidylinositol. The addition of 5-hydroxytryptamine resulted in an increase in the accumulation of label in intracellular inositol 1:2-cyclic phosphate, inositol 1-phosphate and free inositol along with an increase in the release of [3H]inositol to the medium and saliva. The release of [3H]inositol to the medium served as a sensitive indicator of phosphatidylinositol breakdown. The release of [3H]inositol was not increased by cyclic AMP or the bivalent-cation ionophore A23187 under conditions in which salivary secretion was accelerated. The stimulation of fluid secretion by low concentrations of 5-hydroxytryptamine was potentiated by 3-isobutyl-1-methylxanthine, which had no effect on inositol release. The stimulation of fluid secretion by 5-hydroxytryptamine was greatly reduced in calcium-free buffer, but the breakdown of phosphatidylinositol continued at the same rate in the absence of calcium. These results support the hypothesis that breakdown of phosphatidylinositol by 5-hydroxytryptamine is involved in the gating of calcium.

scholarly journals The relationship of calcium to receptor-controlled stimulation of phosphatidylinositol turnover. Effects of acetylcholine, adrenaline, calcium ions, cinchocaine and a bivalent cation ionophore on rat parotid-gland fragments

1975 ◽  
Vol 148 (3) ◽  
pp. 479-485 ◽  
Author(s):  
L M Jones ◽  
R H Michell
Keyword(s):  
Parotid Gland ◽  
De Novo ◽  
Head Group ◽  
Ionophore A23187 ◽  
Bivalent Cation ◽  
Phosphatidylinositol Turnover ◽  
Rat Parotid Gland ◽  
Muscarinic Cholinergic ◽  
Rat Parotid ◽  
Stimulation Of

The possibility that Ca2+ ions are involved in the control of the increased phosphatidylinositol turnover which is provoked by alpha-adrenergic or muscarinic cholinergic stimulation of rat parotid-gland fragments has been investigated. Both types of stimulation provoked phosphatidylinositol breakdown, which was detected either chemically or radiochemically, and provoked a compensatory synthesis of the lipid, detected as an increased rate of incorporation of 32Pi into phosphatidylinositol. Acetylcholine had little effect on the incorporation of labelled glycerol, whereas adrenaline stimulated it significantly, but to a much lower extent than 32P incorporation: this suggests that the response to acetylcholine was entirely accounted for by renewal of the phosphorylinositol head-group of the lipid, but that some synthesis de novo was involved in the response to adrenaline. The responses to both types of stimulation, whether measured as phosphatidylinositol breakdown or as phosphatidylinositol labelling, occurred equally well in incubation media containing 2.5 mm-Ca2+ or 0.2 mm-EGTA [ethanedioxybis(ethylamine)-tetra-acetic acid]. Incubation with a bivalent cation ionophore (A23187) led to a small and more variable increase in phosphatidylinositol labelling with 32Pi, which occurred whether or not Ca2+ was available in the extracellular medium: this was not accompanied by significant phosphatidylinositol breakdown. Cinchocaine, a local anaesthetic, produced parallel increases in the incorporation of Pi and glycerol into phosphatidylinositol. This is compatible with its known ability to inhibit phosphatidate phosphohydrolase (EC 3.1.3.4) and increase phosphatidylinositol synthesis de novo in other cells. These results indicate that the phosphatidylinositol turnover evoked by alpha-adrenergic or muscarinic cholinergic stimuli in rat parotid gland probably does not depend on an influx of Ca2+ into the cells in response to stimulation. This is in marked contrast with the K+ efflux from this tissue, which is controlled by the same receptors, but is strictly dependent on the presence of extracellular Ca2+. The Ca2+-independence of stimulated phosphatidylinositol metabolism may mean that it is controlled through a mode of receptor function different from that which controls other cell responses. Alternatively, it can be interpreted as indicating that stimulated phosphatidylinositol breakdown is intimately involved in the mechanisms of action of alpha-adrenergic and muscarinic cholinergic receptor systems.

scholarly journals Effect of insulin, catecholamines and calcium ions on phospholipid metabolism in isolated white fat-cells

1980 ◽  
Vol 186 (3) ◽  
pp. 781-789 ◽  
Author(s):  
J. Adolfo García-Sáinz ◽  
John N. Fain
Keyword(s):  
Fatty Acids ◽  
Phosphatidic Acid ◽  
Inhibitory Effect ◽  
Phospholipid Metabolism ◽  
Ionophore A23187 ◽  
Fat Cells ◽  
Adrenergic Stimulation ◽  
White Fat ◽  
Adrenergic Activation ◽  
Rat Fat Cells

The incorporation of [32P]Pi into phosphatidylinositol by rat fat-cells was markedly increased in the presence of adrenaline. Phosphatidic acid labelling was also increased, but to a lesser extent. These effects are due to α1-adrenergic stimulation since they were unaffected by propranolol, blocked by α-blockers in the potency order prazosin«phentolamine<yohimbine and mimicked by methoxamine. The α-adrenergic stimulation of phosphatidylinositol labelling did not require extracellular Ca2+, which supports the hypothesis that an increased turnover of phosphatidylinositol is involved in α-adrenergic activation of Ca2+ entry. Insulin and the ionophore A23187 gave a small increase in 32P labelling of phosphatidylinositol in Ca2+-free medium containing 1mm-EGTA. The increases due to insulin or ionophore A23187 were abolished if 2.5mm-Ca2+ was added to medium containing EGTA. However, the increases in labelling of phosphatidylinositol due to α-adrenergic amines were still evident in medium containing EGTA and Ca2+. Lipolytic agents such as corticotropin, dibutyryl cyclic AMP, adrenaline in the presence of phentolamine and isoproterenol decreased [32P]Pi incorporation into phosphatidylinositol, phosphatidylethanolamine and phosphatidic acid. This inhibitory effect may be secondary to accumulation of intracellular unesterified fatty acids, since it was decreased by incubating fewer cells in medium with 6 rather than 3% albumin and was restored by the addition of oleate to the medium. The incorporation of [32P]Pi into phosphatidylcholine was unaffected by lipolytic agents. The data suggest that there is an inhibition of the synthesis of certain phospholipids in the presence of lipolytic agents, which may be secondary to intracellular accumulation of unesterified fatty acids.

scholarly journals Calcium ions modulate hormonally stimulated progesterone production in isolated ovarian cells

1982 ◽  
Vol 202 (2) ◽  
pp. 381-386 ◽  
Author(s):  
J D Veldhuis ◽  
P A Klase
Keyword(s):  
Cyclic Amp ◽  
Calcium Ions ◽  
Ionophore A23187 ◽  
Bivalent Cation ◽  
Progesterone Production ◽  
Ovarian Cells ◽  
Deficient Medium ◽  
Time Periods ◽  
Short Time ◽  
Stimulation Of

Swine granulosa-luteal cells incubated in Ca2+-deficient medium (5 muM final Ca2+ concentration) for short time periods produced diminished quantities of progesterone in response to lutropin. Maximally stimulating effects of prostaglandin E2 and L-adrenaline were also impaired significantly. Diminished progesterone production could not be attributed to alterations in protein synthesis or cell viability. Under Ca2+-deprived conditions, the stimulatory actions of cholera toxin, 3-isobutyl-1-methylxanthine and 8-bromo cyclic AMP were also significantly impeded. Administration of a presumptive antagonist of transmembrane Ca2+ influx (verapamil) or of EGTA to chelate extracellular Ca2+, significantly decreased the total cellular content of Ca2+, and antagonized the actions of lutropin. Micromolar concentrations of trifluoperazine mimicked the suppressive effects of Ca2+ deprivation. Conversely, the bivalent-cation ionophore, ionophore A23187, significantly augmented the stimulation of progesterone produced by lutropin. Thus the present observations implicate Ca2+ in the modulation of hormonally stimulated progesterone production in isolated ovarian cells, and suggest that Ca2+ may influence one or more processes distal to, or independent of, cyclic AMP generation. In addition, the susceptibility of progesterone biosynthesis to inhibition by trifluoperazine suggests a possible role for calmodulin in the ovary.

Adrenergic stimulation of rat resistance arteries affects Ca2+ sparks, Ca2+ waves, and Ca2+oscillations

2001 ◽  
Vol 280 (5) ◽  
pp. H2399-H2405 ◽  
Author(s):  
Joseph R. H. Mauban ◽  
Christine Lamont ◽  
C. William Balke ◽  
W. Gil Wier
Keyword(s):  
Laser Scanning ◽  
Laser Scanning Microscopy ◽  
Confocal Laser ◽  
Resistance Arteries ◽  
Adrenergic Stimulation ◽  
Arterial Diameter ◽  
Low Levels ◽  
Adrenergic Activation ◽  
Cellular Ca ◽  
Stimulation Of

Confocal laser scanning microscopy and fluo 4 were used to visualize local and whole cell Ca2+ transients within individual smooth muscle cells (SMC) of intact, pressurized rat mesenteric small arteries during activation of α1-adrenoceptors. A method was developed to record the Ca2+ transients within individual SMC during the changes in arterial diameter. Three distinct types of “Ca2+signals” were influenced by adrenergic activation (agonist: phenylephrine). First, asynchronous Ca2+ transients were elicited by low levels of adrenergic stimulation. These propagated from a point of origin and then filled the cell. Second, synchronous, spatially uniform Ca2+ transients, not reported previously, occurred at higher levels of adrenergic stimulation and continued for long periods during oscillatory vasomotion. Finally, Ca2+sparks slowly decreased in frequency of occurrence during exposure to adrenergic agonists. Thus adrenergic activation causes a decrease in the frequency of Ca2+ sparks and an increase in the frequency of asynchronous wavelike Ca2+ transients, both of which should tend to decrease arterial diameter. Oscillatory vasomotion is associated with spatially uniform synchronous oscillations of cellular [Ca2+] and may have a different mechanism than the asynchronous, propagating Ca2+ transients.

scholarly journals The effect of intracellular calcium ions on adrenaline-stimulated adenosine 3′:5′-cyclic monophosphate concentrations in pigeon erythrocytes, studied by using the ionophore A23187

1976 ◽  
Vol 158 (2) ◽  
pp. 211-221 ◽  
Author(s):  
A K Campbell ◽  
K Siddle
Keyword(s):  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Time Course ◽  
Ionophore A23187 ◽  
Atp Content ◽  
Bivalent Cation ◽  
Intact Cells ◽  
Maximum Inhibition ◽  
Partial Reversal ◽  
Stimulation Of

1. The bivalent cation ionophore A23187 was used to increase the intracellular concentration of Ca2+ in pigeon erythrocytes to investigate whether the increase in cyclic AMP content caused by adrenaline might be influenced by a change in intracellular Ca2+ in intact cells. 2. Incubation of cells with adrenaline, in the concentration range 0.55--55 muM, resulted in an increase in the concentration of cyclic AMP over a period of 60 min. The effect of adrenaline was inhibited by more than 90% with ionophore A23187 (1.9 muM) in the presence of 1 mM-Ca2+. This inhibition could be decreased by decreasing either the concentration of the ionophore or the concentration of extracellular Ca2+, and was independent of the concentration of adrenaline. 3. The effect of ionophore A23187 depended on the time of incubation. Time-course studies showed that maximum inhibition by ionophore A23187 was only observed when the cells were incubated with the ionophore for at least 15 min before the addition of adrenaline. 4. The inhibition by ionophore A23187 depended on the concentration of extracellular Ca2+. In the absence of Mg2+, ionophore A23187 (1.9 muM) inhibited the effect of adrenaline by approx. 30% without added Ca2+, by approx. 66% with 10 muM-Ca2+ and by more than 90% with concentrations of added Ca2+ greater than 30 muM. However, even in the presence of EGTA [ethanedioxybis(ethylamine)tetra-acetate](0.1--10 mM), ionophore A23187 caused an inhibition of the cyclic AMP response of at least 30%, which may have been due to a decrease in cell Mg2+ concentration. 5. The addition of EGTA after incubation of cells with ionophore A23187 resulted in a partial reversal of the inhibition of the effect of adrenaline. 6. Inclusion of Mg2+ (2 mM) in the incubation medium antagonized the inhibitory action of ionophore A23187. This effect was most marked when the ionophore A23187 was added to medium containing Mg2+ before the addition of the cells. 7. The cellular content of Mg2+ was decreased by approx. 50% after 20 min incubation with ionophore A23187 (1.9 muM) in the presence of Ca2+ (1 mM) but no Mg2+. When Mg2+ (2 mM) was also present in the medium, ionophore A23187 caused an increase of approx. 80% in cell Mg2+ content. Ionophore A23187 had no significant effect on cell K+ content. 8. Ionophore A23187 caused a decrease in cell ATP content under some conditions. Since effects on cyclic AMP content could also be shown when ATP was not significanlty lowered, it appeared that a decrease in ATP in the cells could not explain the effect of ionophore A23187 on cyclic AMP. 9. Ionophore A23187 (1.9 muM), with 1 mM-Ca2+, did not enhance cyclic AMP degradation in intact cells, suggesting that the effect of ionophore A23187 on cyclic AMP content was mediated through an inhibition of adenylate cyclase rather than a stimulation of cyclic AMP phosphodiesterase. 10. It was concluded that in intact pigeon erythrocytes adenylate cyclase may be inhibited by intracellular concentrations of Ca2+ in the range 1-10 muM.

Adrenergic Stimulation of Regional Plasminogen Activator Release in Rabbits

1992 ◽  
Vol 68 (05) ◽  
pp. 545-549 ◽  
Author(s):  
W L Chandler ◽  
S C Loo ◽  
D Mornin
Keyword(s):  
Lower Extremity ◽  
Plasminogen Activator ◽  
Beta Blocker ◽  
Time Course ◽  
Vascular System ◽  
Adrenergic Stimulation ◽  
Epinephrine Administration ◽  
Adrenergic Antagonist ◽  
Vascular Beds ◽  
Stimulation Of

SummaryThe purpose of this study was to determine whether different regions of the rabbit vascular system show variations in the rate of plasminogen activator (PA) secretion. To start, we evaluated the time course, dose response and adrenergic specificity of PA release. Infusion of 1 µg/kg of epinephrine stimulated a 116 ± 60% (SD) increase in PA activity that peaked 30 to 60 s after epinephrine administration. Infusion of 1 µg/kg of norepinephrine, isoproterenol and phenylephrine had no effect on PA activity. Pretreatment with phentolamine, an alpha adrenergic antagonist, blocked the release of PA by epinephrine while pretreatment with the beta blocker propranolol had no effect. This suggests that PA release in the rabbit was mediated by some form of alpha receptor.Significant arterio-venous differences in basal PA activity were found across the pulmonary and splanchnic vascular beds but not the lower extremity/pelvic bed. After stimulation with epinephrine, PA activity increased 46% across the splanchnic bed while no change was seen across the lower extremity/pelvic bed. We conclude that several vascular beds contribute to circulating PA activity in the rabbit, and that these beds secrete PA at different rates under both basal and stimulated conditions.

Activation of Hageman Factor by α-Adrenergic Stimulation

1970 ◽  
Vol 23 (03) ◽  
pp. 417-422 ◽  
Author(s):  
D. G McKay ◽  
J.-G Latour ◽  
Mary H. Parrish
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Adrenergic Receptor ◽  
Adrenergic Stimulation ◽  
Hageman Factor ◽  
Intravascular Coagulation ◽  
Receptor Sites ◽  
High Doses ◽  
Stimulation Of

SummaryThe infusion of epinephrine in high doses produces disseminated intravascular coagulation by activation of Hageman factor. The effect is blocked by phenoxybenz-amine and is therefore due to stimulation of α-adrenergic receptor sites.

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