Sensors for antidiuresis and thirst—osmoreceptors or CSF sodium detectors?

Abstract

Change in sodium concentration of lateral ventricle CSF caused by intracarotid infusion of hypertonic solutions was measured in conscious sheep. Intracarotid infusion (1.6 ml/min) of 1 M NaCl, 2 M sucrose or 4.6 M or 2 M urea caused progressive increase of CSF sodium concentration, whereas 2 M glucose, 2 M galactose or 0.15 M NaCl did not. Of these solutions, only intracarotid 1 M NaCl or 2 M sucrose caused rapid water intake or rapid decrease in free water clearance. 2 M urea caused relatively slow antidiuresis and no water intake. 4.6 M urea which produced the largest rise of CSF[Na] caused slow antidiuresis and inconsistent small water intake. Infusion into a lateral ventricle (0.05 ml/min) of 0.35 M NaCl or 0.7 M sucrose, or fructose, made up in artificial CSF (0.15 M Na) or 0.5 M NaCl alone, all rapidly elicited an antidiuresis and water drinking, whereas intraventricular infusion of pure non-saline 1 M sucrose of 0.7 M urea in CSF was ineffective. Intraventricular 0.35 M NaCl in CSF caused greater antidiuretic and dipsogenic effects than intraventricular 0.7 M sucrose or fructose in CSF. It is postulated that a dual osmoreceptor-sodium sensor system may participate in regulating antidiuretic hormone secretion and thirst, and that the osmoreceptor system mediates the rapid antidiuresis and water drinking caused by intracarotid 1 M NaCl or 2 M sucrose, and is probably located in a brain region without a blood-brain barrier.