Figure 5.

Pharmacological agents which modify blood pressure through actions on vascular smooth muscle cell membrane ion channels.A – Drugs which lower blood pressure. Potassium channel openers (e.g. pinacidil) open ATP-sensitive K⁺ channels and increase diffusion of K⁺ out of the cell. K⁺ efflux hyperpolarizes the cell membrane which triggers closure of voltage-gated calcium channels and a fall in intracellular Ca⁺⁺ concentration. Ca⁺⁺ channel blockers (e.g. Nifedipine, diltiazem, verapamil) block voltage-gated Ca⁺⁺ channels directly, thus also reducing intracellular Ca⁺⁺. A fall in intracellular Ca⁺⁺ reduces the interaction between actin and myosin, lowers arteriolar smooth muscle tone and hence causes a fall in blood pressure. B – Drugs which raise blood pressure. Drugs which block ATP-sensitive K⁺ channels (e.g. glibenclamide) reduce K⁺ efflux from the cell which results in depolarization of the cell membrane and triggers opening of voltage-gated Ca⁺⁺ channels. Ca⁺⁺ influx through these channels increases intracellular Ca⁺⁺ which in turn promotes actin–myosin interactions and an increase in arteriolar tone. K⁺ channel blocking agents may have a role in the treatment of hypotension in septic or haemorrhagic shock.