Osmoregulation of Vasopressin Secretion and Thirst in Health and Disease

Baylis, P. H.; Thompson, Christopher J.

doi:10.1111/j.1365-2265.1988.tb03704.x

Cited by 137 publications

(79 citation statements)

References 116 publications

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“…In patients with osmoreceptor dysfunction, a state similar to CDI can be present without polydipsia, and instead presents with severe dehydration and hypernatremia due to lack of thirst and decreased water intake [57,58]. Thirst is both regulated directly via the osmoreceptor mechanism discussed above, as well as a result of angiotensin II's effect on the thirst center [59].…”

Section: Central Diabetes Insipidus (Cdi)mentioning

confidence: 99%

Diabetes Insipidus: A Review

Shapiro¹

2013

J Diabetes Metab

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Section: Central Diabetes Insipidus (Cdi)mentioning

confidence: 99%

Diabetes Insipidus: A Review

Shapiro¹

2013

J Diabetes Metab

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“…In contrast to the small changes in plasma osmolality required for AVP release, 2-3% increases in plasma osmolality are necessary to induce thirst sensation [3]. As changes in plasma osmolality are within 1-2% of the basal level under most conditions due to the antidiuretic action of AVP, these small changes are below the threshold of thirst [2].…”

mentioning

confidence: 99%

Adipsia increases risk of death in patients with central diabetes insipidus

et al. 2014

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Arginine vAsopressin (Avp) is an antidiuretic hormone which is synthesized in the supraoptic and paraventricular nuclei in the hypothalamus, and released into the systemic circulation from the posterior pituitary [1,2]. Secretion of AVP is precisely controlled by plasma osmolality so that even as little as 1% increases in plasma osmolality or serum sodium levels significantly increase plasma AVP levels [1,2]. Increases in plasma osmolality are sensed via the osmoreceptors in the hypothalamus, and induce not Abstract. Central diabetes insipidus (CDI) is caused by deficiency of arginine vasopressin, an antidiuretic hormone. Patients with CDI manifest polyuria which is usually compensated for by increases in water intake. However, some patients are not able to sense thirst due to the destruction of osmoreceptors in the hypothalamus. These adipsic CDI patients are easily dehydrated and the consequent dehydration could be life-threatening. The objective of this study was to investigate the prognosis of adipsic CDI patients. We have reviewed 149 patients with CDI in three hospitals using databases of the electronic medical recording systems, and examined whether adipsia could affect the morbidity and mortality in CDI patients with multivariable analyses. Twenty-three patients with CDI were adipsic while the remaining 126 patients were non-adipsic. The multivariate analyses showed that the incidence of serious infections which required hospitalization was significantly higher in the adipsic CDI patients compared to that in non-adipsic CDI patients (p <0.001). A total of 6 patients with CDI died during the follow-up (median duration; 60 months, range 1 to 132 months). Four of them were adipsic, three of whom died of infection. The statistical analyses revealed that the risk of death in adipsic CDI patients was significantly higher than in non-adipsic patients (p =0.007). It is thus suggested that adipsic CDI patients were susceptible to serious infections which could be the causes of death.

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“…Destruction of this area of the brain abolishes both AVP secretion and thirst responses to hyperosmolality in experimental animals 3 and in human subjects with brain damage that infarcts the region around the OVLT, who typically are unable to maintain normal plasma osmolalities even under basal conditions. 4 In contrast to the effects of such lesions to eliminate both osmotically stimulated thirst and AVP secretion, diabetes insipidus caused by destruction of the magnocellular AVP neurons in the supraoptic (SON) and paraventricular (PVN) nuclei eliminates dehydration-induced AVP secretion but not thirst, clearly indicating that osmotically stimulated thirst must be generated proximally to the AVP-secreting cells themselves (Figure 1A). Other regions have also been reported to contain putative osmoreceptors, including the hepatic portal circulation, leading to the suggestion that osmoreceptors are widely distributed.…”

Section: Where Are Osmoreceptors Located?mentioning

confidence: 99%

How Does the Brain Sense Osmolality?

Verbalis

2007

Journal of the American Society of Nephrology

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Osmoregulation of Vasopressin Secretion and Thirst in Health and Disease

Cited by 137 publications

References 116 publications

Diabetes Insipidus: A Review

Diabetes Insipidus: A Review

Adipsia increases risk of death in patients with central diabetes insipidus

How Does the Brain Sense Osmolality?

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