Disturbed fluid and electrolyte homoeostasis following dehydration in elderly people

Phillips, P.A., Johnston, C.I. and Gray, L. (1993) Disturbed fluid and electrolyte homoeostasis following dehydration in elderly people. Age and Ageing, 22 1: S26-S33. doi:10.1093/ageing/22.suppl_1.S26

Author Phillips, P.A.
Johnston, C.I.
Gray, L.
Title Disturbed fluid and electrolyte homoeostasis following dehydration in elderly people
Journal name Age and Ageing   Check publisher's open access policy
ISSN 0002-0729
Publication date 1993-01-01
Year available 1993
Sub-type Article (original research)
DOI 10.1093/ageing/22.suppl_1.S26
Open Access Status Not yet assessed
Volume 22
Issue 1
Start page S26
End page S33
Total pages 8
Place of publication Oxford, United Kingdom
Publisher Oxford University Press
Language eng
Abstract Disturbances in homoeostatic capacity are typical of the ageing process. Changes in the neuroendocrine controls of salt and water homoeostasis with age make elderly people more susceptible to fluid and electrolyte disturbances such as dehydration and overhydration. Not only do elderly subjects show reduced thirst and water intake following dehydration, but their kidneys are less able to retain water. This reduced thirst and water intake is not dependent on palatability of the liquids offered as the amounts drunk are no different if water alone or a variety of beverages are offered to healthy elderly dehydrated men. It is of interest that the arginine vasopressin (AVP) response to dehydration is maintained in elderly subjects, indicating that their reduced renal water retentive capacity is due to relative renal resistance to vasopressin. The mechanism underlying the reduced thirst is unclear. Dehydration causes plasma hypertonicity and reduced extracellular fluid (ECF) volume, both of which stimulate thirst and AVP secretion. Elderly subjects show deficits in sensing the reduced ECF volume through reduced low and high pressure baroreceptor sensitivity. In contrast, while the AVP responses to hypertonicity are maintained, the thirst responses seem to be reduced. It seems unlikely that the primary sensing 'osmoreceptor' neurons in the hypothalamus leading to AVP secretion or thirst would be differentially affected by age. Therefore the thirst deficit may result from changes with age in the more poorly defined pathways that bring thirst to consciousness. Following rehydration, thirst and AVP secretion are inhibited in young individuals thus avoiding overhydration. This occurs not only by replacing the water deficit but also more immediately via oropharyngeal sensors that inhibit thirst and AVP secretion immediately upon drinking before water is absorbed. These oropharyngeal sensors also seem changed by ageing as dehydration-induced AVP secretion is not inhibited as effectively by drinking in elderly as in young subjects. These changes in neuroendocrine homoeostatic mechanisms, as well as other renal changes with ageing, predispose even healthy elderly individuals to fluid and electrolyte disorders when excessive salt and water losses or exogenous intake (e.g. intravenous fluid administration) occur.
Keyword Atrial natriuretic peptide
Arginine vasopressin
Geriatric patients
Water deprivation
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: School of Medicine Publications
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Created: Thu, 10 Mar 2011, 01:25:17 EST