:<unk>  effect Mechanism Cellular response Classicalfunctions Vessel tone ↑cAMP, ↓ET-1↓Ca2+, ↑K+ ↓SMC proliferation↑Vasodilation Antiproliferative ↑cAMP ↑PPARgamma ↓Fibroblast growth↑Apoptosis Antithrombotic ↓Thromboxane-A2↓PDGF ↓Platelet aggregation↓Platelet adherence to vessel wall Novelfunctions Antiinflammatory ↓IL-1, IL-6↑IL-10 ↓Proinflammatory cytokines↑Antiinflammatory cytokines Antimitogenic ↓VEGF↓TGF-β ↓Angiogenesis↑ECM remodeling As mentioned above,<unk>  <unk>  is released by healthy endothelial cells and performs its function through a paracrine signaling cascade that involves G protein-coupled receptors on nearby platelets and endothelial cells. The platelet Gs protein-coupled receptor<unk>  receptor) is activated when it binds to<unk> . This activation, in turn, signals adenylyl cyclase to produce cAMP. cAMP goes on to inhibit any undue platelet activation (in order to promote circulation) and also counteracts any increase in cytosolic calcium levels that would result from thromboxane A2 (TXA2) binding (leading to platelet activation and subsequent coagulation).<unk>  also binds to endothelial<unk>  receptors, and in the same manner, raises cAMP levels in the cytosol. This cAMP then goes on to activate protein kinase A (PKA). PKA then continues the cascade by promoting the phosphorylation of the myosin light chain kinase, which inhibits it and leads to smooth muscle relaxation and vasodilation. It can be noted that<unk>  and TXA2 work as physiological antagonists.
Prostacyclin
Endothelin
Angiotensin II 
Prostaglandin
Vasopressin 
Vasopressin
Endrin
Endothelium-derived relaxing factor