Reserpine

Reserpine is a medication derived from the roots of certain plant species, primarily Rauwolfia serpentina. It belongs to the class of antihypertensive drugs known as sympatholytics or adrenergic neuron blockers. Reserpine works by depleting the stores of catecholamines (such as norepinephrine) in nerve endings, resulting in a decrease in sympathetic nervous system activity and thus lowering blood pressure. It is an alkaloid from the roots of Rauwolfia Serpentina (Sarpgandha) : It produces slowly developing fall in BP and bradycardia, taking 2-3 weeks for full effect. The hypotensive action is primarily due to depletion of N.A. from peripheral adrenergic nerve endings.

Indications

-Reserpine is primarily used in the treatment of hypertension (high blood pressure). It may also be prescribed for the management of certain psychiatric disorders, such as schizophrenia, due to its sedative and tranquilizing effects. -Hypertension, hypertensive emergencies and toxaemia of pregnancy.

Dosage

0.25-0.5 mg daily; increased to 1-1.5 mg if required. Injection : 1-2 mg i.m. once or twice daily till oral therapy is possible.

Contra-Indications

Peptic ulcer, history of depressive illness especially in elderly, epileptics & during pregnancy. Parkinson’s disease, thyrotoxicosis, pheochromocytoma.

Special Precautions

Gastritis or gall stones,asthma, bronchitis, lactation, cardiac failure, arteriosclerosis, bradycardia, myocardial infarction, arrhythmia.

Side Effects

Depression, suicidal tendency, dia-rrhoea, increased acid secretion in stomach and miosis, weight gain, nasal stuffiness & impotence. Postural hypotension.

Drug Interactions

Effect of alcohol on CNS & CVS enhanced. Hypotension with levodopa, fenfluramine, phenothiazine & ephedrine. Pressor effect of phenylephrine & catecholamines potentiated. CNS excitation with MAOIs. Lowers seizure threshold in epileptics. Marked myocardial depression with halothane. Hypotensive effects enhanced by thiazide diuretics. Enhance effect of some beta-blockers & increase risk of cardiac glycoside toxicity. Antagonised by sympathomimetic amines & tricyclic antidepressants. Increased p