Bretylium

Bretylium initially enters sympathetic nerve terminals and promotes norepinephrine release through a mechanism that is not yet fully defined, transiently causing increased blood pressure and tachycardia. After several hours, bretylium accumulates within nerve terminals and inhibits vesicular norepinephrine release, producing sympathetic blockade and thereby reducing the heart's responsiveness to sympathetic stimulation, making arrhythmias related to abnormal depolarization less likely to be triggered. In cardiac myocytes, bretylium also inhibits delayed rectifier potassium channels, prolonging phase 3 repolarization of the action potential, slowing the rate of repolarization, and reducing the likelihood of re-entry arrhythmias.