Platelet prostanoid receptors.

  title={Platelet prostanoid receptors.},
  author={Roma A. Armstrong},
  journal={Pharmacology \& therapeutics},
  volume={72 3},
  • R. Armstrong
  • Published 1996
  • Biology, Medicine
  • Pharmacology & therapeutics

Platelet Thromboxane Receptors: Biology and Function

This chapter will review recent progress in definition of the structure and function of the receptor to which TXA2_binds, and of post-receptor signaling pathways in platelets and other cells, and summarize current understanding of the platelet TXA1 receptor.

Activation of the murine EP3 receptor for PGE2 inhibits cAMP production and promotes platelet aggregation.

It is suggested that local production of PGE2 during an inflammatory process can modulate ensuing platelet responses, and loss of the EP3 receptor in a model of venous inflammation protects against formation of intravascular clots.

P2Y12 receptor blockade synergizes strongly with nitric oxide and prostacyclin to inhibit platelet activation

It is demonstrated that PGI2 and NO synergize with P2Y12 receptor antagonists to produce powerful platelet inhibition and the concept of refining ex vivo platelet function testing by incorporating an assessment of endothelial function to predict thrombotic outcomes better and adjust therapy to prevent adverse outcomes in individual patients is introduced.

Combination of cyclic nucleotide modulators with P2Y12 receptor antagonists as anti‐platelet therapy

Endothelium‐derived prostacyclin and nitric oxide elevate platelet cyclic nucleotide levels and maintain quiescence. We previously demonstrated that a synergistic relationship exists between cyclic

P2Y12 and EP3 antagonists promote the inhibitory effects of natural modulators of platelet aggregation that act via cAMP

The ability of the P2Y12 antagonists cangrelor, ticagrelor and prasugrel active metabolite (PAM), and the EP3 antagonist DG-041 to promote the inhibitory effects of modulators of platelet aggregation that act via cAMP is investigated.

Comparison of Anti-Aggregatory Effects of PGI2, PGI3 and Iloprost on Human and Rabbit Platelets

The rank orders of agonist potency are different in rabbit compared to those of human, which indicates that the prostacyclin receptors of rabbit platelets are pharmacologically different from those ofhuman.

Prostacyclin and Its Receptors

This work describes the development of prostacyclin analogues and their role in the enteric nervous system and the characterisation of IP-receptors in the central nervous system.



Epoprostenol (prostacyclin, PGI2) binding and activation of adenylate cyclase in platelets of diabetic and control subjects.

This work suggests that hyperaggregability of diabetic platelets is not due to any alteration of platelet prostacyclin receptor numbers or their activation.

Cellular Activation of Thromboxane Receptors a

An F prostaglandin isomer, 8-epi-PGF2 alpha, which exerts its biological effects through a thromboxane (or closely related) receptor, which can be generated in a free radical-catalyzed or cyclooxygenase-dependent manner.

Prostaglandins and thromboxanes.

This chapter discusses major advances in prostaglandin chemistry and biological activity and indicates the extent to which research has progressed towards the realization of earlier hopes of the discovery of new therapeutic agents.

Prostaglandin endoperoxide analogues which are both thromboxane receptor antagonists and prostacyclin mimetics

The results indicate that EP 035 and EP 157 inhibit the aggregation of human platelets by acting as agonists at the PGI2 receptor linked to adenylate cyclase.

Identification of platelet receptors for prostaglandin I2 and D2.

A binding assay has been developed for platelet prostaglandin receptors using TH]PGEl as ligand and the close competition between PGEl and PGI, for the binding site defined by C3H] PGEl is consistent with recognition of the same receptor by these two prostag landins.