[1] Large clinical trials have shown that combined treatment with reserpine plus a thiazide diuretic reduces mortality of people with hypertension.
[6] The antihypertensive actions of reserpine are largely due to its antinoradrenergic effects, which are a result of its ability to deplete catecholamines (among other monoamine neurotransmitters) from peripheral sympathetic nerve endings.
[11] A 2016 Cochrane review found reserpine to be as effective as other first-line antihypertensive drugs for lowering of blood pressure.
[15] Moreover, reserpine was included as a secondary antihypertensive option for patients who did not achieve blood pressure lowering targets in the ALLHAT study.
[16] It was previously used to treat symptoms of dyskinesia in patients with Huntington's disease,[17] but alternative medications are preferred today.
[21] High dose studies in rodents found reserpine to cause fibroadenoma of the breast and malignant tumors of the seminal vesicles among others.
Early suggestions that reserpine causes breast cancer in women (risk approximately doubled) were not confirmed.
[22] It may produce an excessive decline in blood pressure at doses needed for treatment of anxiety, depression, or psychosis.
Unprotected neurotransmitters are metabolized by MAO (as well as by COMT), attached to the outer membrane of the mitochondria in the cytosol of the axon terminals, and consequently never excite the post-synaptic cell.
[28] Reserpine was isolated in 1952 from the dried root of Rauvolfia serpentina (Indian snakeroot),[29] which had been known as Sarpagandha and had been used for centuries in India for the treatment of insanity, as well as fever and snakebites[30] — Mahatma Gandhi used it as a tranquilizer.
A 2003 review showed barely any evidence that reserpine actually causes depression in either human patients or animal models.
Similarly to tetrabenazine, reserpine, via depletion of monoamine neurotransmitters, produces depression-like effects and lack of motivation or fatigue-like symptoms in animals.