The effects of systemic infusions of the avian antidiuretic hormone arginine vasotocin on water intake of domestic ducks were investigated under steady conditions of water balance in which angiotensin II was effective as a dipsogen. The study proceeded from the consistent stimulatory effect of arginine vasotocin on angiotensin II-responsive neurons found in the subfornical organ of ducks, suggesting brain-intrinsic vasotocinergic control of these neurons which are also accessible to circulating agents because of the lacking blood-brain barrier. Levels of circulating arginine vasotocin of about 2700 pg.ml-1 which were close to the threshold for activation of subfornical organ neurons in vitro, induced weak but significant drinking responses. Even at this high arginine vasotocin level circulatory effects were absent, thereby excluding their interference with water intake. Arginine vasotocin plasma levels of about 60 pg.ml-1 significantly attenuated the dipsogenic action of angiotensin. While drinking in response to high pharmacological levels of arginine vasotocin is assumed to mimic a stimulatory innervation of angiotensin-responsive subfornical organ neurons by brain-intrinsic vasotocinergic axons, attenuation of angiotensin-induced drinking by high physiological arginine vasotocin levels cannot be explained by its action on central neurons, but may be secondary to body fluid retention caused by the antidiuretic action of arginine vasotocin.

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