Abstract
Aquaporin-2, a water-channel protein, is known to increase water permeability due
to vasopressin binding to V2 receptors at the renal collecting duct and is excreted
into the urine. It is still unclear whether a hyponatremic state is caused by vasopressin-dependent
aquaporin-2 in patients clinically diagnosed with the syndrome of inappropriate secretion
of antidiuretic hormone. To determine this, we measured urinary aquaporin-2 and vasopressin
by radioimmunoassay in normonatremic or hyponatremic patients after cerebral infarction
and in healthy controls. In the normonatremia group, urinary aquaporin-2 and plasma
AVP levels were higher than in controls. In the hyponatremia group, plasma AVP was
relatively high despite low plasma osmolality in each patient. However, urinary aquaporin-2
in hyponatremia was significantly increased when compared with the other two groups.
In conclusion, AQP-2 increment does not directly reflect non-osmotic AVP secretion
in a hyponatremic state. This result indicates that the urinary excretion of AQP-2
is not only AVP-dependent in hyponatremic states.
Key words
AQP-2 - AVP - SIADH - Non-Osmotic Stimulation - Cerebral Vascular Disease
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J. Takagi
Department of Laboratory Medicine · Aichi Medical University ·
21-Karimata, Nagakute · Aichi 480-1195 · Japan ·
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