The defence of plasma osmolality

The studies reported in this abstract are the result of various tests of osmosensitivity and sodium sensitivity on drinking, vasopressin secretion and sodium excretion in dogs before and after discrete lesions of the OVLT. A successful lesion was defined as destruction of 95% of the OVLT without significant damage to periventricular tissue. Destruction of the OVLT elevated the threshold increase in plasma osmolality required to elicit drinking to intravenous infusion of hypertonic NaCl from 8 +/- 2 to 23 +/- 2 mosmol/kg H2O, and reduced water intake at these threshold osmolalities from 43 +/- 4 to 15 +/- 3 ml/kg. The water intake following 24 h of water, but not food, deprivation was 36 +/- 7 before the lesion and 43 +/- 9 ml/kg following, volumes which did not differ statistically. However, the effect of 24 h water deprivation on plasma osmolality and sodium excretion was altered by OVLT lesions. In control dogs, water deprivation increased plasma osmolality from 301 +/- 2 to 308 +/- 2 mosm/kg, plasma vasopressin from 2.0 +/- 0.3 to 6.8 +/- 1.3 pg/ml and plasma renin activity from 3.3 +/- 1.2 to 10.4 +/- 3.0 ng AI/ml/3 h and a natriuresis of 2 mEq of sodium/kg. Following OVLT lesions, water deprivation did not result in natriuresis. Furthermore, plasma osmolality increased from 314 +/- 7 to 331 +/- 6 mosmol/kg, vasopressin from 1.6 +/- 0.5 to 5.3 +/- 1.0 pg/ml and PRA from 9.6 +/- 2.4 to 18.2 +/- 5.4 ng AI/ml/3 h. The increase in plasma vasopressin was small in relation to the large rise in plasma osmolality.(ABSTRACT TRUNCATED AT 250 WORDS)