The effect of drinking on atrial natriuretic peptide, vasopressin and thirst appreciation in hyperosmolar man

Abstract

Objectives: To assess whether drinking and oropharyngeal stimuli mediate the release of plasma atrial natriuretic peptide (ANP) in man.

Design: Hypertonic saline was infused into male volunteers to stimulate thirst. In order to avoid any effect of volume change on ANP release, the studies were performed with the subject in the seated position.

Subjects: Seated normal male volunteers (n = 6) were infused with hypertonic saline at a rate of 0.06 ml/kg/min for 90 min on two separate occasions. After a 15-min equilibrium period, subjects were allowed to drink for the following 45-min period on one occasion, but no drinking was permitted on the other occasion.

Measurements: Aliquots of blood were withdrawn at 30-min intervals for 90 min during hypertonic saline infusion, and +3, 6, 9, 12, 15, 30 and 45 min during the drinking/control period for the measurement of plasma ANP, plasma vasopressin, plasma osmolality, serum sodium and haematocrit; thirst was assessed at the same time points using a visual analogue scale. Blood pressure was measured at 15-min intervals.

Results: Hypertonic saline infusion induces increases in plasma vasopressin, plasma osmolality, serum sodium and thirst appreciation (P less than 0.005), and blood volume (P less than 0.05) on both study days; there was no increase in plasma ANP during hypertonic saline infusion. During the drinking period there was the expected decrease in plasma vasopressin (P less than 0.01), plasma osmolality (P less than 0.05), serum sodium (P less than 0.05) and thirst appreciation (P less than 0.01); no significant changes occurred in plasma atrial natriuretic peptide, mean arterial blood pressure or haematocrit during either the drinking or the control period.

Conclusions: The drinking-mediated inhibition of thirst appreciation and plasma vasopressin is not associated with any change in plasma ANP concentrations; it does not appear that oropharyngeal stimuli contribute to the release of ANP in man.