Abstract
The interaction of two coexisting transmitters in the cat submandibular gland has been elucidated by studying effects of VIP and carbachol on cyclic AMP accumulation in isolated acini from the gland. Carbachol was found to potentiate the cyclic AMP increase induced by VIP by an atropine sensitive mechanism. The effect of carbachol on cyclic AMP accumulation was abolished by including EGTA in the incubation medium as was the carbachol mediated potentiation of VIP responses. The calmodulin inhibitor trifluoperazine had a similar, but less marked effect. The effect of carbachol was mimicked by phenylephrine (30 microM) and by the calcium inophore A 23187 (3 microM), and also by ethanol in a concentration reported to enhance membrane fluidity. The phospholipase A2 inhibitor, mepacrine, tended to decrease carbachol actions. Our results show that the potentiation of VIP responses in feline submandibular gland is calcium-dependent. The mechanism could involve a calcium-calmodulin-induced stimulation of adenylate cyclase or calcium-induced change in membrane phospholipid metabolism.
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