Abstract

Salt adapted ducks were intravenously infused with a NaCI load of 0.4 mosm.min-1 a~ministered as solutions of 2000, I000, 500, 250 mosm.kgat rates of 0.2, 0.4, 0.8, 1.6 ml.min -I. The aim of the study was, to see whether a minimum serum osmolality can be defined as threshold for salt gland activation at conditions in which salt balance can be establishe~ by the kidneys. As a rule, infusion with i000 mosm. kg preceded one or more infusions of different osmolalities. Formation of salt gland fluid and urine and their osmolalities were continuously monitored. When steady states of salt gland and urine excretion had established at a given infusion, Na + , K § and CIconcentrations were measured in the salt gland fluid and urine over 30-60 min, and in a blood sample together with serum osmolality. At each type of infusion, salt gland and renal excretion matched the osmotic load within • at steady state conditions. Urine flow increased from 0.04 ml.min -I at 2000 mosm.kg -I infusion to 1.13 ml.min -I at infusion with 250 mosm.kg -~ . During infusions with 500 and 250 mosm-kg -I NaCI, the animals retained water; serum osmolality decreased, sometimes below the level maintained by normally hydrated ducks, but without cessation of salt gland secretion. Even at the lowest serum osmolalities observed during 250 mosm.kg -I infusion (<290 mosm.kg-1) the salt glands still excreted 50% of the infused load. In the urine, the Na/K ratio changed from 3.4 during infusion at I000 mosm.kg -I to 25.9 at 250 mosm.kg -I and was reduced to 8.9 by subsequent infusion of 1.6 ml.min -I of hyposmotic glucose. The results do not indicate the existence of a fixed osmotic threshold for salt gland activation. Renal effects of the mineralocorticoids may be involved in the adjustment of salt excretion between the salt glands and the kidneys.

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