Interactions between alcohol and cardiovascular medications

Alcohol Health & Research World,  Summer, 1990  by Barbara A. Thomas,  Timothy J. Regan

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Clonidine

Clonidine lowers blood pressure by acting on adrenergic receptors located in the brainstem. Alcohol and clonidine are physiologic antagonists (Abdel-Rahman 1989): clonidine depresses activity in the central sympathetic nervous system (the brain and spinal cord), whereas alcohol enhances sympathetic activity. Also, clonidine increases reflex heart rate in response to signals originating from pressure sensors, whereas alcohol impairs this reflex response.

Studying hypertensive rats, Abdel-Rahman (1989) found that doses of clonidine followed by intravenous administration of alcohol in amounts similar to moderate drinking led to a significant reversal of clonidine's hypotensive effect (that is, the effect of lowering blood pressure), and to a brief increase in blood pressure. Szmigielski and colleagues (1989) found that both single doses of alcohol and chronic alcohol use diminished the sensitivity of receptors (in the brains of rats) to clonidine. This effect lasted about 12 hours in the case of a single alcohol dose and at least 48 hours in the case of prolonged alcohol use.

Abdel-Rahman (1989) suggested that inadequate control of blood pressure in hypertensive patients who use alcohol regularly may, in part, be the result of alcohol-clonidine antagonism. Methyldopa and guanabenz also are reported to interact with alcohol (Shinn and Shrewsbury 1988), probably through similar mechanisms.

Guanethidine and Reserpine

Guanethidine and reserpine act on the periperhal nervous system, that is, nerves located outside the brain and spinal cord. Both medications interfere with the movement of norepinephrine (a chemical messenger known as a neurotransmitter) at nerve endings, thereby interrupting the transmission of nerve impulses (Burbank 1987).

Green and Egle (1983) studied the effects of acetaldehyde, the alcohol metabolite, and guanethidine on hypertensive rats. They found that the effects of acetaldehyde varied in accordance with its dosage and with the form of the administration of guanethidine (acute or chronic). Doses of acetaldehyde given intravenously following a single dose of guanethidine led to substantial increases in blood pressure. When acetaldehyde was given to animals who received prolonged administration of guanethidine, it produced two types of responses. At low doses, acetaldehyde raised blood pressure, but less so than acetaldehyde administered after a single dose of guanethidine. At high doses, acetaldehyde decreased blood pressure in rats administered guanethidine chronically. These findings suggest that alcohol may counteract the effect of single doses of guanethidine, yet produce the opposite result in patients receiving prolonged guanethidine treatment.

The effects of reserpine are known to be intensified by alcohol use (American Society of Hospital Pharmacists 1984); the mechanisms involved are probably similar to those of the alcohol-guanethidine interaction.

ANTICOAGULANT AND PLATELET-INHIBITING