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Introduction Pulmonary hypertension PH is a haemodynamic and pathophysiological state including a number of vascular diseases found in multiple clinical conditions, leading to right ventricular failure. The presence of phosphodiesterase-5 PDE 5 in the pulmonary vasculature provides the basis for targeted treatment of pulmonary arterial hypertension PAH with PDE 5 inhibitors.
Endogenous ligands such as nitric oxide NO and natriuretic peptides stimulate pulmonary vasodilatation by use of a common signalling pathway that involves generation of cyclic guanosine monophosphate cGMP as a second messenger to mediate the intracellular effects that finally result in vasodilatation.
The phosphodiesterases PDEs form a family of enzymes PDE 1-11 with different modes of regulation, localization, cellular expression, and inhibitor sensitivities that selectively catalyze the hydrolysis and thereby the degradation of cyclic adenosine monophosphate and cGMP.