THE AVIAN SALT GLAND

Summary 1. Since the electrolyte concentrating capacity of the avian nephron is insufficient to excrete all of the ingested electrolyte when the bird consumes hyperosmotic drinking water, an extra‐renal pathway is necessary to maintain homeostasis. 2. In birds living in coastal and estuarine environments, and in terrestrial environments where the available drinking water is also hyperosmotic with respect to their body fluids, paired salt glands situated in the orbits have evolved as extra‐renal excretory organs. 3. These excretory organs wax and wane functionally in species that migrate between these environments where there is an abundance of freshwater. 4. This functional development of the glands involves the synthesis of new protein and the differentiation of additional excretory tissue that is reflected in the overall growth of the gland. 5. When activated, the glands secrete a fluid containing high concentrations of Na+, Cl‐ and K+ and during prolonged periods of exposure to hypertonic drinking water the birds are able to excrete sufficient quantities of these ingested ions to permit them to remain in positive water balance. 6. The mechanisms responsible for producing the characteristic hyperoosmotic fluid discharged by the activated salt glands appear to be located at two sites: (a) in the principal cells of the secretory tubules, where there is a ouabain‐sensitive Na+‐K+‐dependent ion transporting system located in the basolateral membranes and a furosemide‐sensitive Na+ and Cl‐ co‐transport mechanism located in the basal membrane, and (b) in the complex system of collecting ducts into which the secretory tubules discharge their fluid; the cells lining the duct also possess a ouabain‐sensitive ion transporting system. 7. In the activated gland the Na+‐transporting system operates intermittently to produce excretory fluid only during periods immediately following the ingestion of hyperosmotic drinking water, and secretion ceases when the bird has gained sufficient osmotically‐free water to maintain homeostasis. 8. The initiation and continuation of salt gland secretion occurs in response to the stimulation of an osmoreceptor, probably located in the cardiac vasculature. 9. Sensory impulses arriving in the central nervous system are relayed via parasympathetic motor neurones to muscarinic receptors in the cells of the secretory tubules; the Na+‐K+ dependent ATP‐ase system located in the basolateral membranes is then activated by a cyclic GMP‐mediated mechanism. 10. Sustained salt gland secretion is also dependent upon activation of the pituitary‐adrenal axis. The corticosteriod hormones secreted as a result of this activation interact with specific cytosolic and nuclear receptor macromolecules in the cells of the secretory tubule. Transcriptional changes are presumed to be necessary for sustained extrarenal excretion. 11. Thyroid hormones and prolactin may also be involved indirectly to support continued extrarenal excretion via the salt glands.