cAMP Levels in Reactive Tissues Around Dimethylpolysiloxane Solid Implants

1985 ◽  
Vol 76 (4) ◽  
pp. 570-573 ◽  
Author(s):  
Angela Faga ◽  
Mario Merlino
Keyword(s):  
Camp Levels ◽  
Solid Implants

Ticlopidine and Clopidogrel (SR 25990C) Selectively Neutralize ADP Inhibition of PGE1-Activated Platelet Adenylate Cyclase in Rats and Rabbits

1991 ◽  
Vol 65 (02) ◽  
pp. 186-190 ◽  
Author(s):  
G Defreyn ◽  
C Gachet ◽  
P Savi ◽  
F Driot ◽  
J P Cazenave ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Adenylate Cyclase ◽  
Direct Effect ◽  
Cyclic Nucleotide ◽  
Camp Accumulation ◽  
Rabbit Platelets ◽  
Camp Levels ◽  
Kinetics Of ◽  
Camp Elevation ◽  
Rat Platelets

SummaryTiclopidine and its potent analogue, clopidogrel, are powerful inhibitors of ADP-induced platelet aggregation. In order to improve the understanding of this ADP-selectivity, we studied the effect of these compounds on PGE1-stimulated adenylate cyclase and on the inhibition of this enzyme by ADP, epinephrine and thrombin. Neither drug changed the basal cAMP levels nor the kinetics of cAMP accumulation upon PGEj-stimulation in rat or rabbit platelets, which excludes any direct effect on adenylate cyclase or on cyclic nucleotide phosphodiesterase. However, the drop in cAMP levels observed after addition of ADP to PGEr stimulated control platelets was inhibited in platelets from treated animals. In contrast, the drop in cAMP levels produced by epinephrine was not prevented by either drug in rabbit platelets. In rat platelets, thrombin inhibited the PGEX-induced cAMP elevation but this effect seems to be entirely mediated by the released ADP. Under these conditions, it was not surprising to find that clopidogrel also potently inhibited that effect of thrombin on platelet adenylate cyclase. In conclusion, ticlopidine and clopidogrel selectively neutralize the ADP inhibition of PGEr activated platelet adenylate cyclase in rats and rabbits.

Synergistic Antiplatelet Effect of Ridogrel, a Combined Thromboxane Receptor Antagonist and Thromboxane Synthase Inhibitor, and UDCG-212, a cAMP-Phosphodiesterase Inhibitor

1993 ◽  
Vol 70 (05) ◽  
pp. 822-825 ◽  
Author(s):  
B Hoet ◽  
J Arnout ◽  
H Deckmyn ◽  
J Vermylen
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Receptor Antagonist ◽  
Phosphodiesterase Inhibitor ◽  
Camp Phosphodiesterase ◽  
Thromboxane Receptor ◽  
Thromboxane Synthase Inhibitor ◽  
Thromboxane Receptor Antagonist ◽  
Synthase Inhibitor ◽  
Camp Levels

SummaryRidogrel, a combined thromboxane receptor antagonist and thromboxane synthase inhibitor (1), inhibits platelet aggregation. Following stimulation with arachidonic acid, cAMP-levels are increased in human platelets preincubated with ridogrel, this is due to the known reorientation of the metabolism of the formed endoperoxides towards adenylate cyclase stimulating prostaglandins.Pretreatment of resting platelets with UDCG-212, a cAMP-phosphodiesterase inhibitor (2), also inhibits platelet aggregation induced by arachidonic acid, concomitant with an increase in cAMP levels, due to an inhibition of its breakdown. Under basal conditions, cAMP also is increased.By combining the two drugs, a more than additive action was observed on platelet aggregation and on both resting and stimulated platelet cAMP content. The appropriate combination may result in a more effective antiplatelet strategy.

Transmembrane Calcium Influx Associated with von Willebrand Factor Binding to GP Ib in the Initiation of Shear-Induced Platelet Aggregation

1993 ◽  
Vol 69 (05) ◽  
pp. 496-502 ◽  
Author(s):  
Yasuo Ikeda ◽  
Makoto Handa ◽  
Tetsuji Kamata ◽  
Koichi Kawano ◽  
Yohko Kawai ◽  
...  
Keyword(s):  
Shear Force ◽  
Calcium Influx ◽  
Fold Increase ◽  
Intracellular Camp ◽  
Recombinant Fragment ◽  
Transmembrane Flux ◽  
Irreversible Aggregation ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Camp Levels

SummaryWe found that the binding of multimeric vWF to GP Ib under a shear force of 108 dynes/cm2 resulted in the transmembrane flux of Ca2+ ions with a two-to three-fold increase in their intracellular concentration ([Ca2+]i). The blockage of this event, obtained by inhibiting the vWF-GP Ib interaction, suppressed aggregation. In contrast, the blockage of vWF binding to GP IIb-IIIa, as well as the prevention of activation caused by increased intracellular cAMP levels, inhibited aggregation but had no significant effect on [Ca2+]i increase. A monomeric recombinant fragment of vWF containing the GP Ib-binding domain of the molecule (residues 445-733) prevented all effects mediated by multimeric vWF but, by itself, failed to support the increase in [Ca2+]i and aggregation. These results suggest that the binding of multimeric vWF to GP Ib initiates platelets aggregation induced by high shear stress by mediating a transmembrane flux of Ca2+ ions, perhaps through a receptor-dependent calcium channel. The increase in [Ca2+]i may act as an intracellular message and cause the activation of GP IIb-IIIa; the latter receptor then binds vWF and mediates irreversible aggregation.

Effects of Prostaglandins, Derivatives of Cyclic 3':5'-AMP, Theophylline, Cholinergic Agents and Colchicine on Clot Retraction in Dilute Platelet-Rich Plasma and Gel-Separated Platelet Test Systems

1977 ◽  
Vol 38 (02) ◽  
pp. 0420-0428 ◽  
Author(s):  
J. L Moake ◽  
P. L Cimo ◽  
K Widmer ◽  
D. M Peterson ◽  
J. R Gum
Keyword(s):  
Platelet Rich Plasma ◽  
Inhibitory Effect ◽  
Fibrin Clot ◽  
Serotonin Release ◽  
Dibutyryl Camp ◽  
Clot Retraction ◽  
Dilute Suspensions ◽  
Cholinergic Agents ◽  
Camp Levels ◽  
Derivatives Of

SummaryIn dilute suspensions of platelet-rich plasma (PRP) or gel-separated platelets (GSP), dibutyryl-cAMP (DBcAMP) and monobutyryl-cAMP inhibited platelet-mediated fibrin clot retraction in concentrations of 2–3 × 10–6M, with complete inhibition at 1–3 × 10–4M. Prostaglandin E1 (PGE1), which inhibited fibrin clot retraction in concentrations greater than 1.5–3 × 10–8M, was a more effective inhibitor than either PGE2 or PGF2α. In the presence of theophylline (10–4M), concentrations of DBcAMP, PGE1 PGE2 and PGF2α necessary to inhibit fibrin clot retraction were reduced 50-fold for DBcAMP and 2.5 to 20-fold for the prostaglandins. In dilute PRP or GSP, inhibition of fibrin clot retraction does not result from inhibition of thrombin-induced platelet aggregation. Thus, compounds which increase platelet cAMP levels result in the inhibition of platelet-mediated fibrin clot retraction, and this inhibitory effect may be mediated, at least in part, through suppression of platelet contractility. Cyclic GMP, dibutyryl-cGMP and carbamylcholine-Cl (which stimulates guanylate cyclase) did not influence fibrin clot retraction, and did not prevent inhibition of fibrin clot retraction by DBcAMP and PGE?. Colchicine, in concentrations known to disrupt platelet microtubules (2.5 × 10–6M to 2.5 x 10–3M), had little inhibitory effect on either fibrin clot retraction or platelet (3H)-serotonin release.

Glycogenolytic rates and cAMP in livers of rats running at different treadmill speeds

1983 ◽  
Vol 245 (3) ◽  
pp. R353-R356
Author(s):  
W. W. Winder ◽  
M. A. Beattie ◽  
E. O. Fuller
Keyword(s):  
Liver Glycogen ◽  
Work Rate ◽  
Curvilinear Relationship ◽  
Camp Concentration ◽  
Running Speed ◽  
Cyclic Monophosphate ◽  
High Degree ◽  
The Relationship ◽  
Camp Levels ◽  
Liver Glycogenolysis

The purposes of this study were to determine the effect of different work rates on the rate of liver glycogenolysis and to determine the relationship between liver adenosine 3',5'-cyclic monophosphate (cAMP) levels and the glycogenolytic rate. Rats were run at treadmill speeds ranging from 10 to 34 m/min up a 15% grade for either 30 or 60 min. Both the magnitude of the decrease in liver glycogen and the increase in hepatic cAMP were dependent on the running speed and the duration of running. At the highest work rate a disproportionate acceleration in the liver glycogenolytic rate was observed compared with that at lower work loads, thus resulting in a curvilinear relationship between work rate and liver glycogenolytic rate. A high degree of correlation was found between the liver glycogenolytic rate and hepatic cAMP concentration (r = 0.98). This observation is consistent with the idea that hepatic glycogenolytic rates are determined by cAMP-mediated mechanisms.

Effects of adenohypophysectomy on cAMP levels in chick embryo thyroid, adrenal and spleen

1978 ◽  
Vol 34 (2) ◽  
pp. 263-263
Author(s):  
R. Ferrand ◽  
J. -F. Renaud ◽  
G. H. Le Douarin
Keyword(s):  
Chick Embryo ◽  
Camp Levels

scholarly journals A GENETICALLY DISTINCT FORM OF CYCLIC AMP PHOSPHODIESTERASE ASSOCIATED WITH CHROMOMERE 3D4 IN DROSOPHILA MELANOGASTER

Genetics ◽  
1979 ◽  
Vol 91 (3) ◽  
pp. 521-535
Author(s):  
John A Kiger ◽  
Eric Golanty
Keyword(s):  
Drosophila Melanogaster ◽  
Cyclic Amp ◽  
Structural Gene ◽  
Regulatory Gene ◽  
Heat Stability ◽  
Normal Female ◽  
Dependent Manner ◽  
Cyclic Amp Phosphodiesterase ◽  
Heat Stable ◽  
Camp Levels

ABSTRACT Two cyclic AMP phosphodiesterase enzymes (E.C.3.1.4.17) are present in homogenates of adult Drosophila melanogaster. The two enzymes differ from one another in heat stability, affinity for Mg++, Ca++ activation and molecular weight. They do not differ markedly in their affinities for cyclic AMP, and both exhibit anomalous Michaelis-Menten kinetics. The more heatlabile enzyme is controlled in a dosage-dependent manner by chromomere 3D4 of the X chromosome and is absent in flies that are deficient for chromomere 3D4. Chromomere 3D4 is also necessary for the maintenance of normal cAMP levels, for male fertility, and for normal female fertility and oogenesis. The structural gene(s) for the more heat-stable enzyme is located outside of chromomeres 3C12-3D4. Whether 3D4 contains a structural gene, or a regulatory gene necessary for the presence of the labile enzyme, remains to be determined.

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