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At least 415 records · Page 23Linked to original sources
PubMed1984

Plasma and cerebrospinal fluid vasopressin and osmolality in relation to thirst.

Conscious dogs chronically implanted with a device for cerebrospinal fluid (CSF) sampling from the anterior 3rd ventricle were submitted to 24 h dehydration. During rehydration by drinking the total water intake ( TWI ) after 16 min was determined in 8 and after 90 min in 14 experiments. Samples were simultaneously drawn to determine the osmolalities (Posm, CSFosm ) and AVP concentrations (PAVP, CSFavp ) of plasma and CSF. After 24 h dehydration all of these parameters were significantly elevated in comparison to euhydrated dogs investigated on 19 occasions. In 8 experiments 60% of the final TWI had been ingested within the first 16 min with no changes of Posm, CSFosm and CSFAVP , but a significant decrease of PAVP at this time. TWI per kg body weight ( TWI X kg-1) after 90 min was significantly correlated with the osmolalities and AVP levels in plasma and CSF prior to rehydration. The decreases of Posm, CSFosm and PAVP, but not of CSFAVP , were significantly correlated with TWI X kg-1. The results indicate that PAVP and CSFAVP are subject to long term control by body fluid tonicity exhibiting a feedback relationship to water intake. In addition, PAVP but not CSFAVP seems to be under short term, possibly nonosmotic, control during water intake.

Animals↗
PubMed1988

[Severe hypernatremia in acquired disorder of thirst and vasopressin regulation].

Three patients with severe adipsic hypernatremia (greater than 171 mmol/l) are presented. In two of them, hypernatremia occurred after the operation of a ruptured aneurysm of the A. communicans anterior, in one patient the cause of the disease remained obscure. Despite high plasma osmolality, all patients had low or undetectable plasma vasopressin levels, even throughout hypertonic saline infusion. Urine concentrating ability was partially maintained, suggesting activation of alternative extra- and intrarenal concentrating mechanisms or increased renal sensitivity to low vasopressin concentration. Nonosmolar stimulation (insulin-induced hypoglycemia) did increase vasopressin concentration only subnormally in the two patients tested. This finding might be due to an extended and complex dysfunction of the anterior hypothalamus rather than to a circumscribed defect of the osmoreceptor/thirst center or the supraoptic nuclei.

Adult↗