Abstract
In birds with a marine habitat the nasal glands are modified into salt glands, able to excrete excess sodium chloride. The nervous control of the salt glands was investigated in the herring gull, Larus argentatus. Normal secretion of the salt gland seems to be released by a nerve reflex involving higher nerve centers and central osmoreceptors. The reflex can be evoked experimentally by intravenous injection of a hypertonic NaCl solution or by increasing the osmotic pressure of the blood in other ways. The gland is innervated from a nerve plexus in the anterior part of the orbit of the eye. Secretion is produced by stimulation of a nerve, probably a branch of the VII cranial nerve, which connects with the plexus. The plexus also receives sympathetic fibers, but no secretion was observed after stimulation of the cervical sympathetic. The gland is stimulated to secrete its osmotically highly concentrated fluid (700–800 mm Na) by Mecholyl and acetylcholine, indicating a parasympathetic innervation as the normal excitatory pathway. The secretion that normally occurs in response to a salt load is blocked by anesthesia. It is also inhibited by atropine, adrenaline or acetazolamide (Diamox).
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