Endotoxin stimulates drinking in rats without changing dehydrational signals controlling thirst.
Intravenous injections of endotoxins from Escherichia coli or Salmonella minnesota stimulate drinking and reduce urinary excretion of water and solutes in rats. E. coli endotoxin (0.15 or 0.45 mg/kg i.v.) stimulated drinking without increasing plasma osmolality or sodium concentration, hematocrit, blood hemoglobin, or plasma protein concentration and without decreasing arterial pressure. Similarly, a dipsogenic dose of S. minnesota endotoxin (0.25 mg/kg i.v.) did not reduce arterial or venous pressures or change heart rate. Blocking the renin-angiotensin system with captopril or blocking histamine receptors with pyrilamine and cimetidine did not reduce drinking or urinary fluid retention caused by E. coli endotoxin. Injections of 10 or 450 ng E. coli endotoxin into a lateral cerebral ventricle increased body temperature but not water intake. In contrast to its stimulatory effect in water-replete rats, E. coli endotoxin (0.45 mg/kg i.v.) inhibited drinking in 24-h water-deprived rats. Thus we find no evidence to support the hypothesis that endotoxin causes thirst by changing known physiological signals of cellular or extracellular dehydration. The mechanism remains unknown.