Reserpine clinical pharmacology
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Abdurahman Khalil, M.D. [2]
Clinical Pharmacology
Reserpine depletes stores of catecholamines and 5-hydroxytryptamine in many organs, including the brain and adrenal medulla. Most of its pharmacological effects have been attributed to this action. Depletion is slower and less complete in the adrenal medulla than in other tissues. The depression of sympathetic nerve function results in a decreased heart rate and a lowering of arterial blood pressure. The sedative and tranquilizing properties of reserpine are thought to be related to depletion of catecholamines and 5-hydroxytryptamine from the brain.
Reserpine, like other rauwolfia compounds, is characterized by slow onset of action and sustained effects. Both cardiovascular and central nervous system effects may persist for a period of time following withdrawal of the drug.
Mean maximum plasma levels of plasma concentrations after a single dose of 0.5 mg of reserpine, administered as two 0.25 mg tablets or as an aqueous solution, peaked after 2.5 hours. The mean peak level was approximately 1.1 ng/ml. The two formulations were found to be bioequivalent. Absolute bioavailability of reserpine, as established by comparison to an intravenous dose, has been reported to be approximately 50%.
Reserpine is extensively bound (95%) to plasma proteins. Reserpine is almost completely metabolized in the body, and only about 1% is excreted as unchanged drug in the urine. No definitive studies on the human metabolism of reserpine have been made. After oral administration, an initial half-life of approximately 5 hours is followed by a terminal half-life of the order of 200 hours. Plasma levels may be measurable 14 days after a single dose. The clinical significance of the long terminal half-life is unknown.[1]
References
- ↑ "RESERPINE TABLET [EON LABS, INC.]". Retrieved 7 March 2014.