Vasodilators, primarily affecting the smooth muscles within arterial and venous walls, are commonly used for hypertension treatment. Medications such as minoxidil and hydralazine primarily target arteries and arterioles, while sodium nitroprusside acts on arterioles and venules. Minoxidil, functioning as a prodrug, is metabolized by hepatic sulfotransferase into its active form, minoxidil sulfate, after oral administration. This metabolite binds to the sulfonylurea receptor (SUR) component of ATP-sensitive potassium channels on smooth muscle cell membranes. This binding triggers the opening of the potassium channel, facilitating the outflow of positively charged potassium ions. The resulting hyperpolarization closes voltage-gated calcium channels and inhibits the influx of calcium ions; with less calcium available for muscle contraction, smooth muscles relax, leading to blood vessel dilation and blood pressure reduction. In hypertensive emergencies, sodium nitroprusside is frequently used as a parenterally administered vasodilator. When metabolized, sodium nitroprusside releases nitric oxide, which diffuses into smooth muscle cells and activates the soluble guanylyl cyclase (sGC) enzyme. The activated enzyme converts guanosine triphosphate (GTP) into cyclic guanosine monophosphate (cGMP). Elevated cGMP levels activate protein kinase G (PKG), which opens potassium channels, inhibits calcium ion influx and reduces intracellular calcium levels. It also activates myosin light chain phosphatase, which dephosphorylates myosin light chains, inhibiting actin-myosin interaction. These combined actions result in smooth muscle relaxation, blood vessel dilation, and decreased resistance and blood pressure. However, it is worth noting that sodium nitroprusside releases cyanide, posing a risk of cyanide poisoning.