What is the effect of sildenafil on patients with PAH?

Sildenafil is a phosphodiesterase type 5 (PDE5) inhibitor that primarily works by enhancing the effect of nitric oxide (NO) in the pulmonary vasculature. In patients with pulmonary arterial hypertension (PAH), sildenafil promotes pulmonary vasodilation, which leads to improved blood flow and reduced pulmonary artery pressure. By inhibiting PDE5, sildenafil increases the levels of cyclic guanosine monophosphate (cGMP), which causes relaxation of smooth muscle in the pulmonary vasculature. This mechanism is critical in managing PAH as it directly addresses the underlying issue of increased vascular resistance within the lungs, leading to a significant improvement in exercise capacity and quality of life for these patients.

The other effects, such as increasing heart rate or causing hypotension, may occur in some instances, particularly in patients with other underlying cardiovascular issues, but they are not the primary therapeutic goals of sildenafil in PAH. Similarly, while sildenafil may have some minor effect on systemic vascular resistance, its primary and most significant therapeutic effect is related to pulmonary vasodilation, making this the correct choice when considering its impact on patients with PAH.