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The class of medications that is commonly used to treat pulmonary arterial hypertension (PAH) by relaxing vascular smooth muscle is indeed Ca2+ channel blockers. These medications work by inhibiting the influx of calcium ions through voltage-gated calcium channels in the smooth muscle cells lining the pulmonary arteries. When calcium levels are reduced, smooth muscle relaxation occurs, leading to vasodilation and a subsequent decrease in pulmonary arterial pressure.

Ca2+ channel blockers are particularly beneficial in patients with a positive vasodilator response during acute testing, allowing for improved exercise capacity and overall clinical outcomes in those with PAH.

While other options listed are also important in the context of treating PAH, they work through different mechanisms. For example, ET-1 receptor antagonists block the effects of endothelin-1, a potent vasoconstrictor, while PDE5 inhibitors enhance the effects of nitric oxide by preventing the breakdown of cyclic GMP, leading to vasodilation. Prostacyclin analogs directly stimulate prostacyclin receptors, promoting vasodilation and inhibiting platelet aggregation. Each of these classes contributes to the management of PAH, but the specific mechanism of action focused on relaxing vascular smooth muscle through calcium regulation is the hallmark of Ca2+ channel blockers.