Central Neural Mechanisms in the Cardiovascular Effects of Ethanol

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Abstract

Ethanol has been the most widely used drug known to man, and its prominent neurobehavioral and neurotoxic effects have been well recognized for millenia. Whereas in moderate doses ethanol alleviates stress, it can also activate various components of the sympathoadrenal axis, which is the primary mediator of the body’s response to increased stress. Blood pressure and heart rate are among the key parameters affected by the stress response, and they also illustrate the dual effectiveness of ethanol. On the one hand, the anxiolytic effects of moderate doses of ethanol may be associated with reduced blood pressure and heart rate (Levenson et al., 1980; Reed and Hanna, 1986), and chronic ethanol consumption has been shown to delay the developmental increase in blood pressure in both normotensive and genetically hypertensive strains of rats (Sanderson et al., 1983; Howe et al., 1989). The finding that acute withdrawal from ethanol is often associated with an increase in blood pressure (Clark and Friedman, 1985) and heart rate (Weise et al., 1985) also suggests that during exposure to ethanol the activity of some structures controlling blood pressure and heart rate may be suppressed. However, the situation may be more complex: according to a recent study in 32 patients undergoing an alcohol detoxification protocol, blood pressure hyperreactivity during withdrawal correlated with a positive family history of hypertension, as well as with a higher alcohol consumption based on a quantity/frequency index (King et al., 1989). This suggests that blood pressure hyperreactivity during withdrawal may actually predict future hypertension.