Abstract
Erythrocyte ouabain-sensitive 86rubidium uptake (as an index of Na+,K+-ATPase activity) as well as passive sodium uptake were measured in a group of young men in response to drinking either nonalcoholic beer (as a control) or the same drink with alcohol (1 ml/kg) added. Plasma alcohol concentration rose to 16.7 mM within 70 min of commencement of drinking. There was no change in uptake of 86rubidium or sodium after 60 min in either the alcohol or control studies. There was a late increase in plasma sodium levels 90 min after alcohol ingestion, attributed to fluid volume contraction following diuresis. In contrast, plasma potassium levels fell after alcohol ingestion. This was associated with a decrease in urinary potassium excretion, hence ascribed to an intracellular shift of potassium ions, a change inconsistent with NA+,K+-ATPase inhibition. It is concluded that acute moderate doses of alcohol do not influence NA+,K+-ATPase activity or passive sodium uptake in circulating erythrocytes. Unless vascular smooth muscle is more sensitive to the effects of alcohol in vitro, these findings make it less likely that inhibition of NA+,K+-ATPase mediates alcohol-related hypertension in man.
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