We studied the control of salt gland secretion in hatchling Chelonia mydas.
The threshold salt load to activate salt secretion was between 400 mu mol
NaCl 100 g bodymass (BM)(-1) and 600 mu mol NaCl 100 g BM-1, which caused a
n increase in plasma sodium concentration of 13% to 19%. Following a salt l
oad of 2700 mu mol NaCl 100 g BM-1, salt gland secretion commenced in 12 +/
- 1.3 min and reached maximal secretory concentration within 2-7 min. Maxim
al secretory rate of a single gland averaged 415 mu mol Na 100 g BM-1 h(-1)
. Plasma sodium concentration and total osmotic concentration after salt lo
ading were significantly higher than pretreatment values within 2 min. Adre
nalin (25 mu g kg BM-1) and the cholinergic agonist methacholine (1 mg kg B
M-1) inhibited salt gland activity. Atropine (10 mg kg BM-1) reversed metha
choline inhibition and stimulated salt gland secretion when administered wi
th a subthreshold salt load. Arginine vasotocin produced a transient reduct
ion in sodium secretion by the active gland, while atrial natriuretic facto
r, vasoactive intestinal peptide and neuropeptide Y had no measurable effec
t on any aspect of salt gland secretion. Our results demonstrated that secr
etion 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 th
e chelonian salt gland.