Regulation of canine platelet function II. Catecholamines

1983 ◽  
Vol 245 (1) ◽  
pp. R100-R109 ◽  
Author(s):  
K. M. Meyers ◽  
L. Y. Huston ◽  
R. M. Clemmons
Keyword(s):  
Arachidonic Acid ◽  
Adrenergic Receptor ◽  
Dense Granule ◽  
Platelet Response ◽  
Receptor Agonists ◽  
Alpha Adrenergic Receptor ◽  
Acid Metabolites ◽  
Induced Aggregation ◽  
The Relationship ◽  
Platelet Shape

The action of epinephrine (E) on canine platelet aggregation is described. Although E did not induce a change in platelet shape or aggregation, potentiation of aggregation induced by the following agents was observed at physiological E concentrations (that is, less than 10 nM/1): arachidonic acid; the dense granule agonists, ADP and serotonin (5-HT); and collagen. Epinephrine-induced potentiation was in part independent of formation of arachidonic acid metabolites, and E potentiated the aggregating action of the bivalent cationophore A23187. Potentiation was inhibited by alpha-adrenergic receptor antagonists phenoxybenzamine, phentolamine, and ergotamine, and mimicked by alpha-adrenergic receptor agonists norepinephrine, clonidine, and in some cases, phenylephrine. The beta-adrenergic receptor agonists isoproterenol and dobutamine inhibited ADP-induced aggregation, and this action was presented by pretreating the platelets with propranolol and dichloroisoproterenol. An augmentation of the aggregation response of platelets to arachidonic acid was observed in blood samples withdrawn when circulating catecholamines were elevated. The physiological implication of epinephrine acting as a gain controller that alters the relationship between actuating signal and the platelet response to an agonist is discussed.

Platelet Aggregation Caused by Dithiothreitol

1984 ◽  
Vol 51 (01) ◽  
pp. 119-124 ◽  
Author(s):  
M B Zucker ◽  
N C Masiello
Keyword(s):  
Shape Change ◽  
Blood Platelets ◽  
Dense Granule ◽  
Metabolic Inhibitors ◽  
Electrophoretic Patterns ◽  
Discernible Effect ◽  
Variable Extent ◽  
Triton X ◽  
Induced Aggregation ◽  
Platelet Shape

SummaryMacIntyre et al. showed that over 1 mM dithiothreitol (DTT) aggregates blood platelets in the presence of fibrinogen; aggregation is not inhibited by prostaglandin E1. We confirmed their data and found that 70 mM 2-mercaptoethanol was also active. DTT- induced aggregation was not associated with platelet shape change or secretion of dense granule contents, was not inhibited by tetracaine or metabolic inhibitors, was prevented at pH 6.5, and prevented, reversed, or arrested by EDTA, depending on when the EDTA was added. DTT did not cause aggregation of thrombasthenic, EDTA-treated, or cold (0° C) platelets, which also failed to aggregate with ADP. Platelets stimulated with DTT bound 125I-labeled fibrinogen. Thus DTT appears to “expose” the fibrinogen receptors. SDS gel electrophoresis of platelet fractions prepared by use of Triton X-114 showed that aggregating concentrations of DTT reduced proteins of apparent Mr 69,000 and 52,000 (probably platelet albumin) and, to a variable extent, glycoproteins Ib, IIb and III. Exposure of unlabeled or 125I- labeled platelets to ADP had no discernible effect on the electrophoretic patterns.

Different Requirement of Intracellular Calcium and Protein Kinase C for Arachidonic Acid Release and Serotonin Secretion in Cathepsin G-activated Platelets

1997 ◽  
Vol 78 (02) ◽  
pp. 919-925 ◽  
Author(s):  
Serenella Rotondo ◽  
Virgilio Evangelista ◽  
Stefano Manarini ◽  
Giovanni de Gaetano ◽  
Chiara Cerletti
Keyword(s):  
Arachidonic Acid ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Dense Granule ◽  
Cathepsin G ◽  
Platelet Response ◽  
Relative Contribution ◽  
Kinase C ◽  
Serotonin Secretion ◽  
Dense Granule Secretion

SummaryPrevious studies have shown that platelet stimulation with cathepsin G rapidly results in cytoplasmic calcium ([Ca2+]j) increase and activation of protein kinase C (PKC). To elucidate the relationship between these two biochemical events and their relative contribution to the regulation of platelet response to cathepsin G, arachidonic acid (AA) release and serotonin (5HT) secretion were studied. Platelets made Ca2+- depleted and -permeable by treatment with A23187 were compared to intact platelets to better dissociate calcium changes from other receptor- stimulated events. AA release elicited by cathepsin G in intact platelets was prevented by the Ca2+ chelator BAPTA; in Ca2+-depleted, -permeable platelets AA was released in direct response to added Ca2+ and was not increased by simultaneous stimulation with cathepsin G. In intact platelets, PKC inhibition by Ro 31-8220 or PKC induction with PMA either enhanced or reduced, respectively, cathepsin G-induced AA release. Both BAPTA and Ro 31-8220 prevented 5HT secretion from intact platelets; however, in Ca2+-depleted, -permeable platelets, cathepsin G was able to evoke 5HT secretion and p47 phosphorylation independently of [Ca2+]j increase, both effects being hampered by Ro 31-8220. Ca2+ and PKC therefore regulate PLA2 activity and 5HT secretion in cathepsin G-stimulated platelets in a different manner: the former is mainly triggered by [Ca2+]j increase, while PKC represents the major factor in determining dense granule secretion.

scholarly journals Involvement of phosphoinositide metabolism in potentiation by adrenaline of ADP-induced aggregation of rabbit platelets

1987 ◽  
Vol 242 (3) ◽  
pp. 841-847 ◽  
Author(s):  
C Lalau Keraly ◽  
J D Vickers ◽  
R L Kinlough-Rathbone ◽  
J F Mustard
Keyword(s):  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Inositol Phosphate ◽  
Phosphoinositide Metabolism ◽  
Beta Adrenergic ◽  
Alpha Adrenergic Receptor ◽  
Rabbit Platelets ◽  
Phosphatidylinositol 4 ◽  
Induced Changes ◽  
Induced Aggregation

Changes in phosphoinositide metabolism were examined in washed rabbit platelets stimulated with 0.5 microM-ADP, 50 microM-adrenaline, or ADP and adrenaline in combination. Adrenaline does not stimulate platelet aggregation when used alone, but does potentiate aggregation stimulated by ADP. In platelets prelabelled with [32P]Pi and [3H]glycerol, adrenaline was found to potentiate the ADP-induced changes in platelet phospholipids, causing larger increases in the amount and labelling of phosphatidylinositol 4-phosphate (PIP) and phosphatidic acid than was observed with ADP alone. The combination of ADP and adrenaline did not produce a greater decrease in phosphatidylinositol 4,5-bisphosphate (PIP2) than was produced by ADP alone. In platelets prelabelled with [3H]inositol, adrenaline potentiated the increases in labelling of inositol phosphate and inositol bisphosphate stimulated by ADP; no increase in inositol trisphosphate labelling was detected with ADP alone or with the combination of ADP and adrenaline. Phentolamine, an alpha-adrenergic-receptor antagonist, blocked potentiation by adrenaline of ADP-induced changes in phosphoinositide metabolism. Propranolol and sotalol, beta-adrenergic-receptor antagonists, augmented the potentiation; this is consistent with the concept that the effect of adrenaline is mediated by beta-adrenergic receptors. The effect of adrenaline on phosphoinositide metabolism appears to be to potentiate the mechanisms by which ADP causes turnover of PIP and possibly degradation of PI, rather than the mechanism by which PIP2 is decreased.

Baroreflex mechanisms buffering alpha-adrenergic agonists in conscious dogs

1987 ◽  
Vol 253 (4) ◽  
pp. H728-H736
Author(s):  
A. M. Fujii ◽  
S. F. Vatner
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Adrenergic Receptor ◽  
Peripheral Resistance ◽  
Conscious Dogs ◽  
Receptor Blockade ◽  
Receptor Agonists ◽  
Alpha Adrenergic Receptor

To determine the relative importance of the mechanisms utilized by the arterial baroreflex in buffering the pressor and vasoconstrictor responses to alpha-adrenergic receptor agonists, we studied responses to norepinephrine and phenylephrine in conscious dogs. The dogs were studied 2-8 wk after instrumentation with aortic catheters and aortic electromagnetic flow probes to measure arterial pressure and cardiac output. Total peripheral resistance was calculated on-line by a digital computer. The dogs were studied after beta-adrenergic receptor blockade (propranolol 1.0 mg/kg) to eliminate the complicating inotropic effects of the agonists studied. Norepinephrine (0.2 microgram/kg bolus) increased mean arterial pressure by 30 +/- 3 mmHg, total peripheral resistance by 51 +/- 4 mmHg . l-1 . min-1, and decreased heart rate by 26 +/- 3 beats/min. After arterial baroreceptor denervation, norepinephrine increased mean arterial pressure by 69 +/- 8 mmHg, total peripheral resistance by 48 +/- 6 mmHg . l-1 . min-1, and heart rate did not change. After ganglionic blockade (hexamethonium 40 mg/kg), norepinephrine increased mean arterial pressure by 76 +/- 3 mmHg, total peripheral resistance by 47 +/- 4 mmHg X l-1 X min-1, and heart rate did not change. Only after elimination of the buffering by heart rate by use of cholinergic receptor blockade (atropine 0.1 mg/kg) or ventricular pacing could buffering of the vasoconstrictor responses to alpha-adrenergic receptor agonists be demonstrated. Thus in conscious dogs the primary mechanism for buffering increases in arterial pressure induced by alpha-adrenergic receptor agonists is compensatory changes in heart rate and cardiac output with little buffering of total peripheral resistance.

scholarly journals Alpha-adrenergic receptor agonists in terms of modern views on glaucoma monitoring and treatment

2019 ◽  
pp. 87-91
Author(s):  
V.P. Erichev ◽  
◽  
S.Yu. Petrov ◽  
A.V. Volzhanin ◽  
D.M. Safonova ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Receptor Agonists ◽  
Alpha Adrenergic Receptor

scholarly journals Induction of human platelet fibrinogen receptors by epinephrine in the absence of released ADP

Blood ◽  
1982 ◽  
Vol 60 (1) ◽  
pp. 71-77 ◽  
Author(s):  
EI Peerschke
Keyword(s):  
Adrenergic Receptor ◽  
Human Platelet ◽  
Creatine Phosphate ◽  
Serotonin Release ◽  
Scatchard Analysis ◽  
Receptor Stimulation ◽  
Alpha Adrenergic Receptor ◽  
Fibrinogen Binding ◽  
Adrenergic Antagonist ◽  
Induced Aggregation

The ability of epinephrine to expose platelet fibrinogen receptors independent of released ADP was assessed using aspirin-treated, gel-filtered platelets. Similar to ADP-induced aggregation, platelet aggregation in response to epinephrine was accompanied by fibrinogen binding. Ten micromolar epinephrine induced a maximum number of platelet fibrinogen receptors in the absence of significant 14C-serotonin release. As indicated by Scatchard analysis, receptors exposed by both epinephrine and ADP had similar affinities for fibrinogen, but epinephrine induced approximately 30% fewer receptors than did ADP. This appears to correlate with the lesser degree of primary aggregation observed with this agent. Studies using phentolamine, a specific alpha-adrenergic antagonist, apyrase, or creatine phosphate/creatine kinase indicate that the exposure of platelet fibrinogen receptors by epinephrine was specific for platelet alpha-adrenergic receptor stimulation and was not the result of released ADP.

scholarly journals Efficacy and potency of alpha adrenergic receptor agonists at inhibiting rat hippocampal CA3 network activity

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Lorraine O'shea ◽  
Sarah Boese ◽  
Ke Xu ◽  
Brian Nelson ◽  
Brianna Goldenstein ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Network Activity ◽  
Receptor Agonists ◽  
Alpha Adrenergic Receptor ◽  
Hippocampal Ca3
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