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Abstract
Both individual cells and organs regulate their volume in response to sustained hypo-osmolality
via solute and water losses. Similar processes occur in the whole body to regulate
the volumes of extracellular fluid (ECF) and intravascular spaces toward normal levels.
Body water losses occur via the phenomena "escape from antidiuresis"; solute losses
occur through the secondary natriuresis induced by water retention. As a result of
resistance to arginine vasopressin (AVP) signaling, escape from antidiuresis is caused
by downregulation of kidney aquaporin-2 expression despite high AVP plasma levels.
Recent data have implicated downregulation of vasopressin V2R as a potential mechanism
of resistance, and suggest that this may be a result of decreased intrarenal angiotensin
II signaling in combination with increased intrarenal nitric oxide and prostaglandin
E2 signaling. The natriuresis that results in volume regulation of the ECF and vascular
spaces is the result of intrarenal hemodynamic changes produced by volume expansion,
but the degree to which these effects are modulated by aldosterone secretion and the
activity of distal sodium cotransporters and channels remains to be elucidated. The
clinical implication of these volume-regulatory processes is that the chronic hyponatremic
state is one of water retention and solute losses from intracellular fluid and ECF
compartments. The degree to which solute losses versus water retention contribute
to hyponatremia will vary in association with many factors, including the etiology
of the hyponatremia, the rapidity of development of the hyponatremia, the chronicity
of the hyponatremia, the volume of daily water loading, and individual variability.
Understanding these volume-regulatory processes allows a better understanding of many
aspects of the conundrum of patients with "clinical euvolemia" and dilutional hyponatremia
from AVP-induced water retention.