9.12 : 抗高血压药物：血管扩张剂

Oral vasodilators primarily target arteries and arterioles.

Minoxidil, a prodrug, is converted into its sulfate metabolite by hepatic sulfotransferase.

The metabolite activates K_ATP in smooth muscle cells, facilitating potassium ion outflow, hyperpolarizing the cell, and closing voltage-gated calcium channels.

This inhibits calcium ion influx, relaxing the smooth muscle, dilating blood vessels, and reducing blood pressure.

Sodium nitroprusside, a parenterally administered vasodilator, targets arterioles and venules.

It releases nitric oxide, activating soluble guanylyl cyclase in smooth muscle cells.

This enzyme converts guanosine triphosphate into cyclic guanosine monophosphate, activating protein kinase G.

Activated PKG inhibits calcium ion influx, lowers intracellular calcium levels, and activates myosin light-chain phosphatase, dephosphorylating myosin light chains, and inhibiting actin-myosin interaction.

Collectively, reduced calcium levels and myosin light chain dephosphorylation cause vasorelaxation, lowering peripheral resistance and blood pressure.