AJP - Renal Physiology, Vol 254, Issue 1 15-F24, Copyright © 1988 by American Physiological Society
Plasma AVP and renal concentrating defect in chloride depletion metabolic alkalosis
L. N. Peterson, D. Sztorc, A. Jamshaid, J. Kucharczyk, D. Bichet and D. Z. Levine
Department of Physiology, University of Ottawa, Ontario, Canada.
These studies were undertaken to determine the effect of chronic chloride
depletion metabolic alkalosis (Cl-DEP-MALK) on water intake, plasma
arginine vasopressin (AVP) levels, and renal concentrating ability.
Cl-DEP-MALK was induced by feeding a chloride-free diet to rats subjected
to gastric drainage and to dogs treated with furosemide. All of the animals
developed a urine concentrating defect, polydipsia, and a persistent
reduction in plasma osmolality. However, AVP release was not suppressed.
The results of osmotic loading experiments in dogs analyzed using either
linear or log-linear models have shown that chronic Cl-DEP-MALK
significantly alters the relation between plasma osmolality and plasma AVP.
In the classic linear analysis the results suggest that Cl-DEP-MALK reduces
the plasma osmolality at which plasma AVP can be detected, i.e., reduced
"threshold," and increases the slope of the plasma osmolality-to-plasma AVP
relation nearly twofold, i.e., increased "sensitivity." Finally, we provide
evidence that the concentrating defect is not related to high water
turnover or deficient endogenous AVP and is therefore nephrogenic.
