Reserpine depletes stores of serotonin and norepinephrine in the brain, adrenal medulla, and other tissues, and reduces the reuptake of catecholamines by adrenergic nerve terminals. The drug binds tightly to catecholamine storage vesicles in the adrenergic neuron, eventually destroying these vesicles so that the terminals cannot concentrate or store norepinephrine or dopamine. The result of reserpine's effects on biogenic amines is sympathetic dysfunction, with a subsequent decrease in peripheral vascular resistance and a lowering of blood pressure often associated with bradycardia. Cardiac output, renal blood flow, and glomerular filtration rate are also decreased. After reserpine is discontinued, the synthesis of new vesicles can restore sympathetic function, but this can take several weeks.
Reserpine produces a tranquilizing effect by depletion of catecholamines in the brain.
Convulsions and extrapyramadal effects have occurred following high doses of reserpine. Respiratory stimulation occurs at small doses and respiratory depression occurs with large doses. Additionally, reserpine-induced adrenergic blockade results in increased parasympathomimetic effects including increased gastric acid secretion, GI hypermotility, and miosis. The drug distributes throughout the body tissues and is completely metabolized in the liver to inactive derivatives. Reserpine that is bound to vesicles cannot be removed with dialysis, indicating that the amount of drug bound to vesicles and the amount present in the medium are not in equilibrium.