Possible Mechanism of Acetaldehyde-induced Noradrenaline Release from Sympathetic Nerve Terminals in Isolated Blood Vessels
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1. Vasoconstrictor responses to acetaldehyde were investigated in isolated and perfused canine intermediate auricular (ear) arteries. 2. Single injections of small doses of acetaldehyde (1-3 mumol) induced vasoconstriction in a dose-related manner and showed no tachyphylaxis. On the other hand, large doses of acetaldehyde (10-30 mumol) frequently caused tachyphylaxis when injected at 10 min intervals. 3. After tyramine treatment, constrictions induced by a large dose of acetaldehyde were consistently restored temporarily. 4. The acetaldehyde-induced vasoconstriction was inhibited by bunazosin, a potent alpha 1-adrenoceptor antagonist. 5. A small dose of imipramine blocked tyramine-induced vasoconstriction, but had no significant influence on noradrenaline (NA)-induced constrictions, and caused slight potentiation of acetaldehyde-induced constrictions. 6. Hydrocortisone treatment did not modify tyramine-induced vasoconstrictions and slightly suppressed NA- and acetaldehyde-induced constrictions but not significantly. 7. It is suggested that acetaldehyde causes a release of NA from a NA store of the sympathetic nerve terminals which is different from the tyramine-sensitive NA store, and that the acetaldehyde-sensitive NA store may be readily filled up with NA from the tyramine-sensitive store.
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PMID: 31624517 PMC: 6787161. DOI: 10.1002/joa3.12227.
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PMID: 2594916 DOI: 10.1007/BF00589898.