Abstract
Publisher Summary This chapter presents studies on the polyuria induced by cortisol excess in the dog. Polyuria is one of the foremost symptoms of spontaneous hyperadrenocorticism in the dog. Two mechanisms have been postulated: either cortisol excess blocks the release of arginine vasopressin (AVP) or it interferes with its renal action. These studies were performed in 7 healthy adult dogs. Water deprivation (WD) was used to investigate urine concentrating ability and plasma AVP release in response to dehydration. Urine was collected by spontaneous micturition. Osmolality of urine (Uosm) and plasma (Posm) was determined by freezing point depression. The results of these studies showed that under normal conditions, WD stimulated the production of strongly hypertonic urine without measurable changes of plasma AVP levels, whereas in the period of Cortisol administration, less hypertonic urine was achieved with higher AVP levels during WD. The administration of lysine vasopressin at the end of the WD period during Cortisol administration had no consistent effect on Uosm. The results of the WD study in the dog with the adrenocortical carcinoma were similar to those found in the experimental dogs. The finding of increases in circulating AVP levels during WD in the period of Cortisol administration concurs with the studies on adrenocortical insufficiency that reported that Cortisol affects the action of AVP. In addition, the administration of AVP, after maximal urinary concentration had been achieved by WD, would have caused a further increase in Uosm if AVP release was the limiting factor.
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