Antidiuretic hormone (ADH) does not always exert its well-known water-retaining action on the kidney (Kleeman, 1972). We have recently demonstrated in sheep that a high salt intake (Burstyn, Horrobin & Manku, 1972) and cortisol treatment (Horrobin, Manku & Burstyn, 1973) can convert the usual sodium-retaining action of aldosterone into a sodium-losing one. Both prolactin and oxytocin can convert aldosterone back into a sodium-retaining substance. We have therefore investigated the possibility that cortisol, prolactin and oxytocin may have interactions with ADH similar to those that they have with aldosterone.
Seven anoestrous Merino ewes were prepared and treated throughout the experiment with a supplement of 80 mequiv. NaCl/day, and urine collections were made as previously described (Burstyn et al. 1972). Each day at 14.00 h an injection of either 15 mu. arginine-vasopressin (Ferring) or of 1 ml isotonic saline was given to each animal through a jugular venous cannula. Preliminary tests had
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