By measuring the release of 86Rb, potassium movement was compared in parasympathectomized (Px) and contralateral control parotid gland slices three weeks following surgical denervation. 2. Carbachol and phenylephrine elicited a biphasic increase in 86Rb release that was dose related and could be blocked by atropine and phentolamine respectively. The transient phase was of 2-4 min duration and Ca independent whereas the sustained phase of 86Rb release was greatly reduced by the omission of the external Ca. 3. Denervation caused a shift to the left of the 86Rb efflux dose-response curve to carbachol and phenylephrine (3.75- and 3.37-fold respectively). Pilocarpine had similar action to carbachol but it behaved as a partial agonist. 4. Parasympathectomy (Px) increased the intrinsic activity of the partial agonist pilocarpine and converted it to a full agonist. Results of the present study indicate the possibility of an altered receptor-signal transduction mechanism between the receptor and phospholipid turnover/Ca mobilization in the denervated rat parotid gland.
