Author(s): Salata RA, Verbalis JG, Robinson AG
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Abstract The act of drinking ameliorates thirst and inhibits the secretion of vasopressin before changes in extracellular fluid volume or osmolality in both animals and man. We evaluated whether this reflex inhibition of vasopressin secretion might be due to the presence of oropharyngeal receptors in humans. After dehydration, normal subjects (n = 4) were allowed to suck on ice chips for 30 min. Despite the absence of changes in plasma sodium (Na+) or osmolality, the mean plasma vasopressin level decreased promptly within 10 min from 2.8 to 1.8 pg/mL, and it remained low for 30 min after ice ingestion. When the dehydration protocol was repeated with the subjects receiving 100 mL water (25 C) for 30 min rather than ice chips, plasma vasopressin levels did not change. These data demonstrate that activation of cold-sensitive oropharyngeal receptors results in inhibition of vasopressin secretion independently of osmotic or gastric factors. In a second study 0.2 mL/kg X min 3\% NaCl was administered for 90 min as a second stimulus to vasopressin secretion, and ice chips were given during the last 30 min of infusion. Plasma vasopressin levels increased steadily to 3.3 +/- 0.5 (+/- SEM) pg/mL by 45 min, and despite ice ingestion increased further to 4.6 +/- 0.8 pg/mL by 90 min. Consequently, hypertonicity appears to be a stronger stimulus to vasopressin release, since the suppressive effect of stimulation of oropharyngeal receptors with ice was not evident during the NaCl infusion. Finally, no changes in vasopressin levels were found in subjects holding concentrated NaCl solutions in their mouths for 30 min, indicating that the oropharyngeal receptors are not responsive to local changes in osmolality. The presence of such cold-sensitive oropharyngeal receptors may explain the desire of severely dehydrated patients, e.g. patients with diabetes insipidus, for cold liquids.
This article was published in J Clin Endocrinol Metab
and referenced in Journal of Diabetes & Metabolism