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Cholinergic-nitrergic transmitter mechanisms in the cerebral circulation
1Department of Pharmacology, Southern Illinois University School of Medicine, Springfield, Illinois 62794-9629, USA. tlee@siumed.edu
Microscopy Research and Technique
|April 13, 2001
Summary
Nitric oxide (NO), not acetylcholine (ACh), primarily causes vasodilation in cerebral arteries. However, ACh may modulate NO release from cholinergic-nitrergic nerves.
Area of Science:
- Neuroscience
- Vascular Biology
- Pharmacology
Background:
- Cerebral blood vessels possess vasodilator nerves.
- Acetylcholine (ACh) was initially proposed as the primary neurotransmitter for cerebral vasodilation.
- Parasympathetic cholinergic nerves innervate cerebral vasculature.
Purpose of the Study:
- To discuss the neuronal origin of nitric oxide (NO) in cerebral arteries.
- To explore the role of ACh in modulating NO release from cholinergic-nitrergic nerves.
- To investigate the mechanisms of neurogenic vasodilation in the brain.
Main Methods:
- Pharmacological studies using isolated cerebral arterial ring preparations.
- Investigation of neurotransmitter roles in vasodilation.
- Analysis of co-release mechanisms.
Main Results:
- Nitric oxide (NO), not ACh, mediates the primary component of neurogenic vasodilation.
- ACh and NO are co-released from the same cholinergic-nitrergic nerves.
- ACh functions as a presynaptic modulator of NO release.
Conclusions:
- The major neurogenic vasodilation in large cerebral arteries is mediated by NO.
- ACh plays a modulatory role in NO release from these nerves.
- Evidence supports the neuronal origin of NO in cerebral vasculature.