Cyclic adenosine monophosphate

Prostacyclin, the other endogenous platelet inhibitor we mentioned, activates the G-protein coupled receptor known as the prostaglandin I2 receptor, usually called the IPR.

This receptor couples to G-alpha-S, and as we learned in previous tutorials, activation of this G-protein pathway increases the intracellular concentration of C-AMP arising from increasing the activity of adenylate cyclase, which increases the conversion of ATP to C-AMP.

C-AMP activates protein kinase A, which has many similar phosphorylation targets as PKG, which are concerned with inhibiting platelet activation.

A key indicator of platelet reactivity is the intracellular concentration of C-AMP.

Higher C-AMP concentrations reduce platelet activity, and lower C-AMP concentrations increase platelet activation.

We will learn how the C-AMP concentration is influenced by other GPCRs in a moment.

With the loss of inhibition from the endothelial layer discussed, it's important to understand how collagen activates platelets, as these two factors work in tandem to lead to platelet activation and subsequent aggregation to form a thrombus.

Initial collagen-platelet interactions are primarily mediated by four different non-GPCRs on the plasma membrane of the platelet.

Choice C, dipyridamole, correct answer.

So dipyridamole is a phosphodiesterase inhibitor, both PDE3 and PDE5, preventing the breakdown of cAMP, cGMP respectively.

And this is gonna result in vasodilation, blood vessels.

cAMP, cGMP both are vasodilatory, especially cGMP.

And the increased cAMP and cGMP also gonna result in decreased platelet aggregation.

Now, cilostazol is a similar medication.

Cilostazol used for peripheral vascular disease prevents the breakdown of cAMP.

So it's a PDE3 inhibitor.