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Nitric oxide and the cerebral vascular function.

T J Lee1

  • 1Department of Pharmacology, SIU School of Medicine, Springfield, IL 62794-9629, USA. tlee@wpsmtp.siumed.edu

Journal of Biomedical Science
|January 25, 2000
PubMed
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Nitric oxide (NO), not acetylcholine (ACh), is the primary transmitter for cerebral vasodilation. NO is coreleased with ACh and VIP, regulating cerebral blood flow in health and disease.

Area of Science:

  • Neuroscience
  • Cardiovascular Physiology
  • Pharmacology

Background:

  • Cholinergic vasodilator innervation of cerebral circulation is known.
  • Acetylcholine (ACh) is present in cerebral blood vessels but is not the primary vasodilator transmitter.

Purpose of the Study:

  • To identify the primary transmitter responsible for cerebral vasodilation.
  • To elucidate the roles of acetylcholine (ACh), vasoactive intestinal polypeptide (VIP), and nitric oxide (NO) in cerebral circulation.

Main Methods:

  • Investigated the corelease of neurotransmitters from cholinergic-nitrergic and VIPergic-nitrergic nerves.
  • Examined the presynaptic modulation of NO release by ACh and VIP.
  • Studied the synthesis and recycling of NO precursors in cerebral vasculature.

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Main Results:

  • Nitric oxide (NO) is the primary transmitter for smooth muscle relaxation and vasodilation.
  • ACh presynaptically inhibits NO release, while VIP facilitates it.
  • A system for L-citrulline recycling to L-arginine for NO synthesis exists in cerebral nerves and endothelial cells.

Conclusions:

  • Neuronal and endothelial NO are critical for regulating cerebral vascular tone and circulation.
  • NO, coreleased with ACh and VIP, is the key mediator of cerebral vasodilation.
  • Understanding NO pathways is vital for managing cerebrovascular health and disease.