Cyclic 3?,5?-adenosine monophosphate level and adenylate cyclase activity in human blood platelets during storage in ACD solution

1977 ◽  
Vol 34 (4) ◽  
pp. 329-332 ◽  
Author(s):  
Evelyne Lammerant-Guillemare ◽  
Fran�oise Corcelle-Cerf ◽  
Jacques Lammerant
Keyword(s):  
Adenylate Cyclase ◽  
Human Blood ◽  
Blood Platelets ◽  
Adenosine Monophosphate ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Human Blood Platelets

Cyclic 3′,5′-Adenosine Monophosphate in Human Blood Platelets

Nature ◽  
1969 ◽  
Vol 224 (5219) ◽  
pp. 609-610 ◽  
Author(s):  
EDWIN W. SALZMAN ◽  
LENA L. NERI
Keyword(s):  
Human Blood ◽  
Blood Platelets ◽  
Adenosine Monophosphate ◽  
Human Blood Platelets

Some Biochemical Studies With SQ 26271: A Stable Partial Prostacyclin Agonist In The Human Platelet

1981 ◽  
Author(s):  
Don N Harris ◽  
Marie B Phillips ◽  
Inge M Michel ◽  
Harold J Goldenberg ◽  
James E Heikes ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Partial Agonist ◽  
Blood Platelets ◽  
Fold Increase ◽  
Primary Phase ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Induced Aggregation

A newly synthesized 9α-homo-9,11-epoxy-5,13-prostadienoic acid analogue, SQ 26271 (8(S)9(S)11(R)12(S)-9,11-epoxy-9α- homo-5(Z),13(E)-15(R)-hydroxyprostadienoic acid) inhibited arachidonic acid (AA)-induced platelet aggregation at concentrations which did not affect thromboxane B2 (TXB2) levels with an I50 value of 0.25 μM. It also was a potent inhibitor of platelet aggregation caused by collagen, 9,11- AzoPGH2, SQ 24810 (9,11-epoxy-9α-homo-5(Z),13(E)-15α- hydroxyprostadienoic acid) and epinephrine (secondary phase). However, it had little or no effect on thromboxane or prostaglandin synthetase activities. Moreover, SQ 26271 also inhibited the primary phase of epinephrine- and ADP- induced aggregation. In addition SQ 26271 caused a 3-fold increase in platelet adenylate cyclase activity, partially blocked prostacyclin stimulated adenylate cyclase activity and caused a 6-fold elevation of cyclic AMP levels in intact platelets, which was blocked by SQ 22536 (9-tetrahy- dro-2-furyl)adenine), an inhibitor of platelet adenylate cyclase activity. Finally, the inhibition of platelet aggregation by SQ 26271 was potentiated by an inhibitor of cyclic AMP phosphodiesterase (SQ 20009, etazolate), and reversed by SQ 22536. The above data indicate that SQ 26271 is a stable partial agonist of the prostacyclin receptor in human blood platelets.

scholarly journals Surface membrane clearing of receptor-ligand complexes in human blood platelets

1987 ◽  
Vol 87 (3) ◽  
pp. 465-472
Author(s):  
O. Behnke
Keyword(s):  
Human Blood ◽  
Blood Platelets ◽  
Surface Membrane ◽  
Adenosine Monophosphate ◽  
Membrane System ◽  
Intercellular Spaces ◽  
Platelet Antibodies ◽  
Internalization Process ◽  
Human Blood Platelets

Human blood platelets were challenged sequentially in vitro with polyclonal anti-platelet antibodies and cationized ferritin. Both ligands bound to the surface membrane and were sequestered by internalization into a surface-connected membrane system (SCS) with a cleared surface membrane as the eventual result. Patching and capping of bound antibody preceded internalization, and platelets cooperated in the clearing process by adhering to each other at capped areas and by mutual covering up, a process dubbed platelet hugging. The internalization process was repeated upon challenge with the second ligand, the two ligands being sequestered as separate deposits in the SCS, mirroring the two cycles of internalization. Platelets were activated during internalization process and tended to aggregate. In aggregates, surfaces exposed to the medium were cleared of ligand, which accumulated in the intercellular spaces and within the SCS of the aggregated platelets. Aggregation but not internalization and hugging was prevented by adenosine and adenosine monophosphate.

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