Sildenafil treats pulmonary hypertension by selectively inhibiting phosphodiesterase type 5 (PDE5). This enzyme normally breaks down cyclic guanosine monophosphate (cGMP), a crucial molecule for smooth muscle relaxation. By blocking PDE5, sildenafil increases cGMP levels.
Elevated cGMP leads to vasodilation–widening of blood vessels in the lungs. This reduces pulmonary vascular resistance, improving blood flow and reducing strain on the heart. The resulting lower pressure in the pulmonary arteries eases breathing and improves exercise tolerance.
Specifically, increased cGMP activates protein kinase G (PKG), triggering a cascade of events that relax pulmonary artery smooth muscle. This mechanism is particularly relevant in pulmonary hypertension, where abnormally constricted arteries significantly increase blood pressure within the lungs.
It’s important to note that sildenafil’s effect is targeted; it primarily affects the pulmonary vasculature, minimizing systemic side effects compared to other vasodilators.
However, individual responses to sildenafil vary. Dosage adjustments are frequently needed to optimize therapy and achieve the best balance between efficacy and tolerability. Close monitoring of blood pressure and other vital signs is therefore crucial.
