AJP - Regulatory, Integrative and Comparative Physiology, Vol 265, Issue 6 1247-R1252, Copyright © 1993 by American Physiological Society
Impairment of osmotically stimulated AVP release in patients with primary polydipsia
A. M. Moses and B. Clayton
Department of Medicine, State University of New York Health Science Center, Syracuse 13210.
The secretion of arginine vasopressin (AVP) from the posterior pituitary is
primarily and finely regulated by the osmolality of plasma. Even though a
number of factors alter osmolality-induced release of AVP, there are no
published data in humans that have addressed the role of chronic
overhydration on this phenomenon. To address this problem we have
identified eight patients with primary polydipsia using criteria not
involving measurement of AVP, and have subjected them to standardized
infusions of hypertonic saline. These patients had less AVP in both plasma
and urine in relation to plasma osmolality than was found in normal
subjects. In addition, their rate of rise of plasma and urine AVP was less
than in normal subjects. Their osmotic threshold for AVP release may have
been higher than normal. These data demonstrate that chronic overhydration
in humans downregulates the release of AVP in response to hypertonicity.
This phenomenon may explain the impairment of urine concentration in
patients with primary polydipsia and emphasizes the basis of the difficulty
that may occur clinically in differentiating between patients with primary
polydipsia and partial central diabetes insipidus.
