Inhaled nitric oxide (iNO) reduces pulmonary vascular resistance by decreasing which of the following ions?

Inhaled nitric oxide (iNO) primarily reduces pulmonary vascular resistance through its action on calcium ions. Nitric oxide is a potent vasodilator that works by promoting the production of cyclic guanosine monophosphate (cGMP) in the smooth muscle cells of blood vessels. cGMP leads to the relaxation of these smooth muscle cells, which reduces the contraction typically induced by increased calcium levels inside the cells.

When calcium is present in the smooth muscle cells, it binds to calmodulin and activates myosin light chain kinase (MLCK), leading to muscle contraction and consequently increased vascular resistance. By decreasing intracellular calcium concentrations or inhibiting calcium's effects through the activation of cGMP pathways, iNO leads to vasodilation and a reduction in pulmonary vascular resistance.

This physiological mechanism is crucial, especially in conditions like pulmonary hypertension where elevated pulmonary vascular resistance contributes to the disease. The other ions listed—magnesium, potassium, and sodium—do not play a direct or primary role in the mechanism of action of inhaled nitric oxide in the context of reducing pulmonary vascular resistance.