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, 2015, 13
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Progress in the Understanding and Management of Pulmonary Arterial Hypertension

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Progress in the Understanding and Management of Pulmonary Arterial Hypertension

A M Chakrabarti et al. Glob Cardiol Sci Pract.

Figures

Figure 1.
Figure 1.
The three key pathways upon which currently licensed treatments for pulmonary arterial hypertension act. The prostacyclin and nitric oxide pathways cause vasodilatation and the endothelin pathway vasoconstriction. Dashed lines indicate omitted steps. Enzymes are coloured green. Therapies are coloured red. Lines ending in a triangle indicate an agonist/potentiator, lines ending in a bar indicate an antagonist/inhibitor. Abbreviations: AC, adenylate cyclase; ATP, adenosine triphosphate; cAMP, cyclic adenosine monophosphate (AMP); cGMP, cyclic guanosine monophosphate (GMP); ECE, endothelin converting enzyme; eNOS, endothelial nitric oxide synthase; ERA, endothelin receptor antagonist; ET-1, endothelin; ETA, endothelin receptor type A; GTP, guanosine triphosphate; IP, prostaglandin I2 receptor; IP3, inositol triphosphate; PDE5I, phosphodiestase (PDE) type 5 inhibitor; PGI2, prostaglandin I2; PGIS, prostaglandin I synthase; PIP2, phosphatidylinositol bisphosphate; PLC, phospholipase C; NO, nitric oxide; sGCS, soluble guanylate cyclase (sGC) stimulator. Adapted from Montani et al. (2014).
Figure 2.
Figure 2.
A timeline of key milestones in the history of pulmonary arterial hypertension. * Date of Food and Drug Administration approval. Abbreviations: BMPR2, bone morphogenetic protein receptor type 2; PAH, pulmonary arterial hypertension; PH, pulmonary hypertension; RCT, randomised controlled trial; WHO, World Health Organisation.

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