The relationship between thirst perception and plasma osmolality was studied during hypertonic and physiological saline infusion in ten healthy volunteers. Thirst perception was quantified using a linear visual analogue scale which volunteers marked at intervals during the infusion periods. Infusion of hypertonic saline caused a steady rise in plasma osmolality together with a progressive linear increase in thirst perception and also plasma arginine vasopressin. No significant changes in thirst, plasma osmolality or plasma arginine vasopressin occurred during infusion of physiological saline. Linear regression analysis of the results defined the functions. Thirst (cm) = 0.3 (plasma osmolality-281) (r = +0.92, P less than 0.001) and plasma arginine vasopressin (pmol/l) = 0.4 (plasma osmolality-285) (r = +0.96, P less than 0.001). The osmolar threshold for thirst onset thus defined (281 mosmol/kg) was much lower than in previous studies and similar to the theoretical osmolar threshold for vasopressin release (285 mosmol/kg). We conclude that thirst perception rises in a progressive fashion throughout a wide range of plasma osmolality and that the osmolar threshold for thirst onset is similar to the theoretical osmolar threshold for vasopressin release. The results are compatible with the concept of either a single osmoreceptor subserving both thirst and vasopressin release, or two osmoreceptors sharing similar functional characteristics.

Studies on intact animals and isolated rat hepatocytes have shown that arginine vasopression (AVP) stimulates glycogen phosphorylase to break down glycogen and raise plasma glucose concentrations. Since no similar work has been performed on healthy human adults, the effect of moderate (25 pmol/min) and high (75 pmol/min) dose AVP infusion on plasma glucose, intermediary metabolites, glucose kinetics, and circulating glucagon and insulin concentrations was investigated. After AVP infusion, plasma glucose rose from 4.9 +/- 0.1 to a peak of 5.7 +/- 0.2 mmol/l (P less than 0.001), but no changes in blood lactate, pyruvate, alanine, glycerol or 3-hydroxybutyrate concentrations were observed. The glucose rise was accounted for entirely by an increase in the rate of appearance of glucose from 11.19 +/- 0.43 to 13.38 +/- 0.63 mu mol/kg/min (P less than 0.001). Infusion of AVP also increased plasma glucagon concentrations from 38 +/- 8 to 79 +/- 20 pg/l (P less than 0.01). The hyperglycaemic effect of AVP may be mediated solely by stimulation of glucagon release, but we cannot exclude direct stimulation of glycogen phosphorylase activity.

Osmoregulation of vasopressin secretion was studied in eight healthy women in the follicular and luteal phases of the menstrual cycle. Basal plasma osmolality in the luteal phase was significantly lower than in the follicular period (282.4 +/- 0.6, 285.6 +/- 1.1mmol/kg, respectively, P less than 0.05). Plasma AVP (pAVP) and plasma osmolality (pOsm) were measured during the infusion of 850 mmol/l saline in both phases of the cycle, and linear regression analyses of these data gave the following regression equations (i) follicular, pAVP = 0.43 (pOsm - 284), r = + 0.93, (ii) luteal, pAVP = 0.31 (pOsm - 279), r = + 0.95. Both the slope and abscissal intercept were significantly different (P less than 0.01). Osmotic threshold for thirst sensation in the luteal phase was lower than the follicular (293 +/- 2,297 +/- 1 mmol/kg, P less than 0.005). We conclude that, in the luteal phase, the threshold for AVP release and the gain or sensitivity of the osmostat are reduced together with lowering of the thirst threshold, which account for the lower basal luteal plasma osmolality.

Drinking rapidly abolishes thirst and vasopressin secretion in dehydrated humans before major changes in plasma osmolality are observed. We studied the effects of drinking on plasma vasopressin and thirst in seven healthy volunteers rendered hypernatremic by the infusion of hypertonic (855 mmol/l) sodium chloride solution. Thirst was measured on a visual analogue scale (0-10 cm). Infusion of hypertonic saline caused linear increases in plasma osmolality (289 +/- 1 to 306 +/- 1 mosmol/kg, mean +/- SE, P less than 0.001), plasma vasopressin (0.6 +/- 0.2 to 6.4 +/- 1.9 pmol/l, P less than 0.001), and thirst (1.4 +/- 0.4 to 7.4 +/- 0.5 cm, P less than 0.001). Water was allowed 15 min after cessation of the infusion, and within 5 min of drinking both plasma vasopressin and thirst were significantly lower than postinfusion. After 20 min of drinking, plasma vasopressin had fallen from 6.5 +/- 0.9 to 1.3 +/- 0.3 pmol/l (P less than 0.001) and thirst from 7.7 +/- 0.5 to 1.0 +/- 0.2 cm (P less than 0.001) despite no significant change in plasma osmolality (306 +/- 0.9 to 304 +/- 0.8 mosmol/kg, P = 0.17), and the drinking of 1,200 +/- 60 ml of water, over 85% of the mean cumulative water intake in the 30-min drinking period. Control studies in the same subjects showed comparable rises in plasma vasopressin, plasma osmolality, and thirst during hypertonic saline infusion but no fall in any of these parameters during an equivalent 30-min period after the infusions, during which water was withheld.(ABSTRACT TRUNCATED AT 250 WORDS)