Clinical Chemistry
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Clinical Chemistry 55: 1909, 2009; 10.1373/clinchem.2009.133777
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Google Scholar
Right arrow Articles by Richardson, R.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Richardson, R.
(Clinical Chemistry. 2009;55:1909.)
© 2009 American Association for Clinical Chemistry, Inc.


Commentaries

Commentary

Robert Richardson

Toronto General Hospital, Toronto, ON, Canada.

Address correspondence to the author at: Toronto General Hospital, 200 Elizabeth St., Toronto, ON, Canada. Fax 416-340-4999; e-mail robert.richardson@uhn.on.ca.

The first 20% of the full text of this article appears below.

Patients with chronic hyponatremia have vasopressin acting on the kidney, causing water retention and dilution of the sodium in the extracellular fluid. In surveys of hospitalized patients with hyponatremia, the stimulus for vasopressin secretion is low effective circulating volume via the baroreceptor in about two-thirds of patients. . . . [Full Text of this Article]







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2009 by the American Association for Clinical Chemistry.