Following the general reduction of extracellular fluid volume by hemorrhage, or the selective reduction of this volume in the thorax by positive pressure breathing, the volume regulating mechanism of the dog is implicated as part of the over-all compensatory mechanism to such stress situations, and appears to be dominant over any regulation via the osmoreceptors. Both these experimental procedures produce characteristic compensatory cardiovascular reactions, depressed renal function and highly significant increases in the circulating level of antidiuretic hormone. Following the isotonic expansion of the extracellular fluid volume with dextran, or selective expansion of the vascular capacity of the thorax by negative pressure breathing, the volume regulating mechanism appears to be subdominant to the control of body fluid volume via the osmoreceptors. In the case of an increase in extracellular fluid volume, reflex responses directed at volume regulation have no statistically significant action on renal hemodynamics, and any action on the release or inhibition of antidiuretic hormone could not be detected with certainty because of the limiting sensitivity of the bio-assay.
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