Abstract
Pekin ducks were implanted with devices allowing intracerebroventricular (i.c.v.) microinfusions at rates of 0.1–0.4 μl/min during 15 min in the conscious animals. When hydrated by intragastric infusion of 1 ml/min tap water, i.c.v. infusion of hypertonic NaCl solutions reduced urine flow and increased osmolality, presumably due to increased ADH release. Osmotically equivalent Li+ salts (Cl, Br, So 4 2− ) caused a slightly prolonged antidiuresis, while Ca2+ and Mg2+ salts caused a more protracted antidiuresis. Urea solution osmotically equivalent to 4.8% NaCl had no effect on diuresis, while osmotically equivalent mannitol solution slightly enhanced diuresis. Angiotensin II (0.5–2.5 pmol in 15 min) and Carbachol (3.0 pmol in 15 min) infused in 0.9% saline caused antidiuresis. The results suggest that the central control of ADH release in birds is similarly organized as in mammals, with receptive elements reacting to ionic rather than osmotic changes and with Na+ as the naturally involved cation. In ducks with their salt glands activated by i.v. infusion of 800 mosmol NaCl/kg H2O at 0.2 ml/min, salt gland secretion was not augmented by i.c.v. microinfusion of hypertonic NaCl but inhibited by i.c.v. infusion of osmotically equivalent mannitol solution. The supraorbital salt glands, when activated appear to be little stimulated further by a rise but may be inhibited by a fall of i.c.v. Na+ concentration.