Osmoregulation of thirst and vasopressin secretion in human subjects: effect of various solutes

Abstract

Various hypertonic solutions were infused in healthy human volunteers to determine their effect on thirst and vasopressin secretion. Hypertonic saline and mannitol produced prompt and parallel increases in plasma osmolality and vasopressin concentration. For both of these solutes, there was a high degree of correlation between these measurements. The slope describing this relationship varied considerably between individuals, but the same subjects showed similar slopes with either saline or mannitol. Both solutions stimulated thirst. Hypertonic urea infusions produced a comparable rise in osmolality but produced a smaller increase in plasma vasopressin and stimulated thirst in only one of the subjects. With urea, the correlation between plasma osmolality and vasopressin was significantly lower. Within individuals, the slope describing this relationship was significantly correlated with that seen during hypertonic saline. Hypertonic glucose significantly increased plasma osmolality but decreased plasma vasopressin and had no detectable effect on thirst. We conclude that osmoregulation of vasopressin in humans is mediated by a selective osmoreceptor that is located primarily outside of the blood-brain barrier and that individual differences in osmoregulatory sensitivity are not solute specific.

Diabetes Insipidus: A Review

“…The OVLT is a circumventricular organ of the brain, outside of the bloodbrain-barrier (BBB) which contains neurons capable of detecting osmolality [5,9,19]. While the MNCs are intrinsically osmosensitive, the OVLT, positioned outside the BBB can sense osmolites such as urea and mannitol, that do not penetrate the BBB [9,28,29]. Additionally the OVLT integrates signals from various hormones including angiotensin II, relaxin, and atrial natriuretic peptide.…”

Effects of chronic, urea-induced osmotic diuresis on kidney weight and function in rats

“…Urea is an endogenous, slightly toxic substance which is also a final metabolite in ureaexcreting animals such as mammals. When used to induce osmotic diuresis, urea does not cause vasopressin secretion, leading several researchers to suggest that urea-induced osmotic diuresis is similar to the osmotic diuresis caused by glucose in the diabetic state [15][16][17]. Because of this similarity, urea was used to induce osmotic diuresis in this study.…”

“…For example, mannitol injections have been used to experimentally induce osmotic diuresis in normal rats [14]. However, osmotic diuresis associated with hyperglycaemia has been shown to be markedly different from osmotic diuresis induced by mannitol or a hypertonic sodium chloride solution [15][16][17]. The increase in plasma osmotic pressure due to hyperglycaemia is unlikely to cause an effective osmotic stimulus at osmoreceptors.…”

“…The increase in plasma osmotic pressure due to hyperglycaemia is unlikely to cause an effective osmotic stimulus at osmoreceptors. Thus, the osmotic diuresis associated with hyperglycaemia does not stimulate vasopressin secretion as does the osmotic diuresis induced by mannitol [15][16][17]. Urea is an endogenous, slightly toxic substance which is also a final metabolite in ureaexcreting animals such as mammals.…”

Thirst perception in dehydrated sickle cell disease patients in steady state

“…al., 1990). The release of arginine vasopressin due to changes in plasma osmolality has been well documented (Baylis and Robertson, 1980;Robertson and Athar, 1976;Zerbe and Robertson, 1983). The extensive series of experiments in which thirst has been investigated in animals has also been documented (Fitzsimons, 1972).…”