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Archives of cardiovascular diseases
Volume 109, n° 10
pages 550-561 (octobre 2016)
Doi : 10.1016/j.acvd.2016.03.004
Received : 7 July 2015 ;  accepted : 31 Mars 2016
Pulmonary arterial hypertension: Basic knowledge for clinicians
Hypertension artérielle pulmonaire : connaissances de base pour les cliniciens
 

Figure 1




Figure 1 : 

Prostacyclin (PGI2) signalling pathway. PGI2 is produced from arachidonic acid metabolites in endothelial cells, and acts on smooth muscle cells through prostacyclin receptor (IP) mediation, which leads to an increase in cyclic adenosine monophosphate (cAMP) concentration, resulting in vasodilation and reduced proliferation. Therefore, one of the pulmonary arterial hypertension-specific therapies is the use of prostacyclin analogues, as they have the ability to mimic prostacyclin signalling in smooth muscle cells. AC: adenylyl cyclase; ATP: adenosine triphosphate.


Figure 2




Figure 2 : 

Endothelin (ET)-1 signalling pathway. ET-1 is released from endothelial cells and acts on smooth muscle cells through the interaction of two types of receptors (ET-1 receptor type A [ET-A] and ET-1 receptor type B [ET-B]), both of which mediate vasoconstriction and proliferation. The use of endothelin-1 receptor antagonists (ERAs) is one of the therapeutic strategies to attenuate pulmonary arterial hypertension, because ERAs can block the ET-1 receptor, albeit with different selectivity, and stop the signalling that leads to further vasoconstriction.


Figure 3




Figure 3 : 

Nitric oxide (NO) signalling pathway. The formation of NO from L-arginine is catalysed by endothelial NO synthase (eNOS). NO is released from endothelial cells, and acts in smooth muscle cells, where it stimulates soluble guanylyl cyclase (sGC) to increase cytoplasmic cyclic guanosine monophosphate (cGMP), which exerts vasodilator and proliferative effects. Phosphodiesterase-5 (PDE-5) is one of the enzymes responsible for the hydrolysis of cGMP, and for that reason it is one of the main therapeutic targets in pulmonary arterial hypertension. Through the use of sGC stimulators and PDE-5 inhibitors, we are able to stimulate the production of cGMP and to slow down its hydrolytic breakdown, respectively, making it available to exert its beneficial effects. GMP: guanosine monophosphate; GTP: guanosine-5′-triphosphate.


Figure 4




Figure 4 : 

Experimental model of monocrotaline-induced pulmonary arterial hypertension (PAH). After monocrotaline injection, rats undergo vascular remodelling and endothelial dysfunction, which lead to a progressive increase in pulmonary vascular resistance (PVR) and, ultimately, to right ventricular hypertrophy (RVH) and increased RV systolic and diastolic pressures, as well as an increase in right atrial area (RAA). Due to the progressive increase in PVR, RV function deteriorates over time and, eventually, the animal dies of RV failure. ESP: end-systolic pressure; EDP: end-diastolic pressure.

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