Drug Interactions between bendroflumethiazide / rauwolfia serpentina and Motrin Cold and Flu

MONITOR: Concomitant use of nonsteroidal anti-inflammatory drugs (NSAIDs) and diuretics may adversely affect renal function due to NSAID inhibition of the renal synthesis of prostaglandins that help maintain renal perfusion in dehydrated states. The risk may be increased in patients on dietary sodium restriction. At the same time, hypotensive effect of the diuretics may be reduced because inhibition of prostaglandins can lead to unopposed pressor activity and, consequently, elevation in blood pressure. Natriuretic and diuretic effects may also be reduced, as NSAIDs have been reported to cause sodium and water retention, which may account for the increased risk of congestive heart failure associated with the combination. One study showed an increase in the incidence density of congestive heart failure (in patients over 55 years of age) from 9.3 per 1,000 person-years in patients on diuretics to 23.3 per 1,000 person-years in patients on both diuretic and NSAID therapy. NSAIDs may also increase the risk of hyperkalemia associated with potassium-sparing diuretics.

MANAGEMENT: In patients receiving both diuretic and NSAID therapy, management consists of avoiding dehydration and carefully monitoring the patient's renal function and blood pressure. If renal insufficiency or hyperkalemia develops, both drugs should be discontinued until the condition is corrected.

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MONITOR: The hypotensive effects of thiazide diuretics and alpha-adrenergic blockers may be additive. Postural hypotension may occur.

MANAGEMENT: Hemodynamic responses should be monitored during coadministration, especially during the first few weeks of therapy. Patients should be advised to take the alpha-blocker at bedtime and to notify their physician if they experience dizziness or syncope while awake.

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MONITOR: Sympathomimetic amines may decrease the hypotensive effect of postganglionic adrenergic blocking agents, while the latter may potentiate the pharmacologic effects of direct-acting sympathomimetic amines (e.g., dobutamine, epinephrine, methoxamine, norepinephrine) but inhibit those that are primarily indirect-acting (e.g., mephentermine). Postganglionic adrenergic blocking agents such as guanadrel, guanethidine, and rauwolfia alkaloids work by depleting catecholamine stores from adrenergic nerve endings. Therefore, they may sensitize adrenergic receptors to direct-acting sympathomimetics, but blunt the effects of indirect-acting agents whose activity is mediated through the release of catecholamines. Guanethidine and reserpine have been reported to attenuate the pharmacologic effects (mydriasis, pressor response) induced by ephedrine and dopamine, both of which exhibit direct and indirect sympathomimetic activities (i.e., mixed-acting). However, guanethidine intensified the mydriasis produced by phenylephrine, which is also thought to be mixed-acting. Conversely, ephedrine has been shown to partially reverse the hypotensive effect of guanethidine.

MANAGEMENT: Due to their pressor effect, sympathomimetic amines should be used cautiously in patients with hypertension. Alternatives to postganglionic adrenergic blocking agents should be considered if patients are treated with sympathomimetic amines, since effects of the latter may be intensified or diminished depending on whether they are direct- or indirect-acting. Most agents with indirect sympathomimetic activity are mixed-acting, thus it may be difficult to predict how they will be affected by postganglionic adrenergic blocking agents. If the combination is used, blood pressure and heart rate should be monitored.

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