Control of salt gland activity in the hatchling green sea turtle, Chelonia mydas
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We studied the control of salt gland secretion in hatchling Chelonia mydas. The threshold salt load to activate salt secretion was between 400 μmol NaCl 100 g bodymass (BM)−1 and 600 μmol NaCl 100 g BM−1, which caused an increase in plasma sodium concentration of 13% to 19%. Following a salt load of 2700 μmol NaCl 100 g BM−1, salt gland secretion commenced in 12 ± 1.3 min and reached maximal secretory concentration within 2–7 min. Maximal secretory rate of a single gland averaged 415 μmol Na 100 g BM−1 h−1. Plasma sodium concentration and total osmotic concentration after salt loading were significantly higher than pretreatment values within 2 min. Adrenalin (25 μg kg BM−1) and the cholinergic agonist methacholine (1 mg kg BM−1) inhibited salt gland activity. Atropine (10 mg kg BM−1) reversed methacholine inhibition and stimulated salt gland secretion when administered with a subthreshold salt load. Arginine vasotocin produced a transient reduction in sodium secretion by the active gland, while atrial natriuretic factor, vasoactive intestinal peptide and neuropeptide Y had no measurable effect on any aspect of salt gland secretion. Our results demonstrated that secretion of the salt gland in C. mydas can be modified by neural and hormonal chemicals in vivo and that the cholinergic and adrenergic stimulation of an exocrine gland do not appear to have the typical, antagonist actions on the chelonian salt gland.
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