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Horm Metab Res 2003; 35(1): 62-66
DOI: 10.1055/s-2003-38393
Original Clinical
© Georg Thieme Verlag Stuttgart · New York

Urinary Excretion of Aquaporin-2 and Inappropriate Secretion of Vasopressin in Hyponatremic Patients after Cerebral Infarction

J.  Takagi 1 , K.  Otake 2 , N.  Nakao 2 , M.  Takashashi 2 , Y.  Hirooka 1
  • 1Department of Laboratory Medicine, Aichi Medical University, Aichi, Japan
  • 2Fourth Department of Internal Medicine, Aichi Medical University, Aichi, Japan
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Publikationsverlauf

Received 31 January 2002

Accepted after revision 29 July 2002

Publikationsdatum:
01. April 2003 (online)

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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 ·

Telefon: + 81 (561) 62-3311 (ext. 2115) ·

Fax: + 81 (561) 62-3075

eMail: jutakagi@aichi-med-u.ac.jp