DRUG INTERACTIONS
Polythiazide
Thiazides may add to or potentiate the action of other antihypertensive drugs. Potentiation occurs with ganglionic or peripheral adrenergic blocking drugs.
Hypokalemia may be more likely to develop during concomitant use of corticosteroids or ACTH. Diuretic-induced hypokalemia may precipitate digitalis toxicity.
Thiazide drugs may augment the paralyzing actions of tubocurarine, and may decrease the arterial responsiveness to norepinephrine. Extra precautions may be necessary in patients who may require these drugs or their derivatives, as in surgery.
Dosage adjustment of antidiabetic agents is frequently indicated during thiazide administration. Indomethacin may partially antagonize the hypotensive effect of the thiazide diuretics. Generally, do not give lithium with diuretics because they reduce lithiums renal clearance and add a high risk of lithium toxicity.
Quinidine, a weak base, may have its half-life prolonged by concomitant administration of thiazide diuretics which alkalinize the urine.
Sulfonamides may potentiate the action of the thiazide diuretics, possibly by displacement from binding sites on plasma albumin.
Orthostatic hypotension may be aggravated by the use of alcohol, barbiturates, or narcotics with thiazide diuretics.
Reserpine
Reserpine should be used cautiously with digitalis or quinidine as the concurrent use may enhance the appearance of arrhythmias.
Additive CNS depressant effects may occur when reserpine is administered concomitantly with other CNS depressants such as barbiturates and alcohol.
Concomitant administration of reserpine and levodopa has been reported to reduce the patient's response to levodopa. Reserpine should be avoided in patients receiving levodopa.
The effects of indirect-acting sympathomimetic amines such as ephedrine may be decreased.
Patients who are receiving monoamine oxidase inhibitors may experience excitation and hypertension when reserpine is added. The combination should be avoided.
Reserpine may add to the pharmacologic effects of beta-adrenergic blocking agents (i.e., CNS depression and cardiovascular effects).
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