Abstract
An investigation of the role of autonomic control in guinea pig nasal mucosa was carried out by neurotransmitter release and computer simulation method.
The nasal mucosa which was removed under pentobarbital anesthesia, was incubated with 3H-NA or 3H-Ach and infused with Krebs-Ringer solution.
The fluids were collected every 2 minutes and were counted by liquid scintillation spectrophotometry.
NA released upon electric stimulation was reduced by Ach in a dose-dependent manner, and this action was inhibited by atropine. Histamine did not induce Ach release from the parasympathetic terminal endings.
Ach had no infuluence of the Ach-release induced by electrical stimulation, but Ach enhanced the spontaneous release of 3H-Ach. We made a micro-computer program that simulates the diffusions of NA and Ach from autonomic terminals to the surface of effector organs, and the bindings to effector organs.
An increase in the number of adrenergic fibers increased the number of NA binding receptors.
An increase in the number of cholinergic fibers increased the number of Ach binding receptors and delayed the beginning of NA binding, and resulted in a decrease in the number of NA-binding receptors. The increase of sensitivity of effector organs and cholinergic receptor in the nerve terminals reduced the number of NA-binding adrenergic receptors, and increased the number of Ach-binding cholinergic receptors.
These results of this study suggested that parasympathetic nervous system seemed to control the ‘timing’ of the beginning of NA binding.
