Renin-aldosterone axis in ethanol intoxication during sodium and fluid repletion versus depletion.
Renin-aldosterone axis in acute moderate ethanol intoxication was studied in four healthy males during sodium depletion and during sodium and volume repletion. Ethanol (1.2 g/kg body wt) was taken orally in supine position at a steady rate for 90 min. In sodium-depleted subjects starting levels of plasma renin activity (PRA) and plasma aldosterone were increased as expected. During ethanol intoxication PRA rose further (p less than 0.001), whereas aldosterone showed a decreasing trend, albeit not significant. Thus, a dissociation between PRA and plasma aldosterone was noticed. Increased serum NA+/K+ ratio (p less than 0.02), or an inhibitory action of ethanol on aldosterone secretion, may explain the broken renin-aldosterone nexus. In the second experiment, the subjects were sodium replete. During ethanol intoxication, 1350-1420 ml isotonic NaCl was infused intravenously to compensate for fluid loss due to alcohol diuresis. In that experiment neither PRA nor plasma aldosterone showed significant changes. Thus, dehydration due to alcohol diuresis appears to be the main reason for increased PRA during ethanol intoxication. As in previous studies increased serum Na+/K+ ratio along with rising blood alcohol concentration was observed, independently of sodium and fluid balance.
D000328:Adult; D000435:Alcoholic Intoxication / Q000097:blood* / Q000503:physiopathology; D000450:Aldosterone / Q000097:blood; D001794:Blood Pressure; D005665:Furosemide / Q000494:pharmacology*; D006339:Heart Rate; D006801:Humans; D008297:Male; D011188:Potassium / Q000097:blood; D012083:Renin / Q000097:blood; D012084:Renin-Angiotensin System / Q000187:drug effects*; D012964:Sodium / Q000097:blood / Q000502:physiology*; D014882:Water-Electrolyte Balance
D000450:Aldosterone; D005665:Furosemide; D012964:Sodium; D012083:Renin; D011188:Potassium