Evidence for presynaptic parasympathetic receptors on nasal blood vessels.
Noradrenergic synapses in the heart and several blood vessels have been shown to possess prejunctional receptors that modulate the release of norepinephrine from the synapse. The present experiment attempted to find evidence for presynaptic receptors for acetylcholine that modulated norepinephrine release. From the evidence obtained, it appears that the acetylcholine released from nasal parasympathetic fibers does not directly affect the smooth muscle of nasal blood vessels. Acetylcholine does, however, appear to inhibit the release of norepinephrine from nasal sympathetic nerve terminals. It appears that any nasal vasodilation produced by nasal parasympathetic fibers is caused by acetylcholine acting on an inhibitory, presynaptic, muscarinic receptor on the sympathetic nerve terminals. Acetylcholine would exert its control over nasal vessels by regulating the degree of sympathetic neurotransmitter release.
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D004285:Dogs; D004558:Electric Stimulation; D006145:Guanethidine / Q000494:pharmacology; D066298:In Vitro Techniques; D009131:Muscle, Smooth, Vascular / Q000502:physiology; D009297:Nasal Mucosa / Q000098:blood supply*; D010275:Parasympathetic Nervous System / Q000502:physiology*; D017981:Receptors, Neurotransmitter / Q000502:physiology; D014661:Vasoconstriction / Q000187:drug effects
D017981:Receptors, Neurotransmitter; D001285:Atropine; D000109:Acetylcholine; D006145:Guanethidine