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Research Article Free access | 10.1172/JCI114804

Hyponatremia in rats induces downregulation of vasopressin synthesis.

A G Robinson, M M Roberts, W A Evron, J G Verbalis, and T G Sherman

Department of Medicine, School of Medicine, University of Pittsburgh, Pennsylvania 15261.

Find articles by Robinson, A. in: PubMed | Google Scholar

Department of Medicine, School of Medicine, University of Pittsburgh, Pennsylvania 15261.

Find articles by Roberts, M. in: PubMed | Google Scholar

Department of Medicine, School of Medicine, University of Pittsburgh, Pennsylvania 15261.

Find articles by Evron, W. in: PubMed | Google Scholar

Department of Medicine, School of Medicine, University of Pittsburgh, Pennsylvania 15261.

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Department of Medicine, School of Medicine, University of Pittsburgh, Pennsylvania 15261.

Find articles by Sherman, T. in: PubMed | Google Scholar

Published October 1, 1990 - More info

Published in Volume 86, Issue 4 on October 1, 1990
J Clin Invest. 1990;86(4):1023–1029. https://doi.org/10.1172/JCI114804.
© 1990 The American Society for Clinical Investigation
Published October 1, 1990 - Version history
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Abstract

Hyponatremia due to inappropriate secretion of vasopressin is a common disorder in human pathophysiology, but vasopressin synthesis during hypoosmolality has not been investigated. We used a new method to quantitate synthesis of vasopressin in rats after 3, 7, and 14 d of hyponatremia induced by administering dDAVP (a vasopressin agonist) and a liquid diet. Vasopressin synthesis was completely turned off by 7 d. Vasopressin mRNA levels in the hypothalamus paralleled the reduction in synthesis and were reduced to levels of only 10-15% of the content in control rats. When hyponatremia was corrected by withdrawal of dDAVP, vasopressin mRNA slowly returned to normal over 7 d. The observation that vasopressin synthesis can be so completely turned off leads to several conclusions: under normal physiological conditions the neurohypophysis is chronically upregulated; there must be an osmotic threshold for initiation of vasopressin synthesis (and release); the large store of hormone in the posterior pituitary is essential for vasopressin to be available during times of decreased synthesis; and, finally, some nonosmolar stimulus for synthesis must be present during clinical disorders when vasopressin is secreted (and synthesized) despite hypoosmolality.

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