title: Cholinergic prejunctional inhibition of nitrergic neurotransmission in the guinea-pig isolated basilar artery.
abstract: 1. The effects of endogenous and exogenous acetylcholine (ACh) on nitrergic relaxations elicited by electrical field stimulation (EFS) were studied in guinea-pig endothelium-denuded basilar artery preparations precontracted with 1 micromol/L prostaglandin F(2 alpha) and a possible role of K+ channels in mediating the effects was investigated. 2. Acetylcholine (3 micromol/L) and physostigmine (10 micromol/L) produced small, yet statistically significant, inhibitions of EFS-induced nitrergic relaxations, while atropine (1 micromol/L) slightly enhanced the nitrergic response. The ACh-induced inhibition was atropine sensitive. Acetylcholine or atropine did not affect relaxations induced by sodium nitroprusside. 3. The inhibition of nitrergic relaxations by 3 micromol/L ACh was prevented by the K+ channel blockers tetraethylammonium and 4-aminopyridine, but was not changed by iberiotoxin, apamin or glibenclamide. 4. Neither vasoactive intestinal polypeptide nor the alpha2-adrenoceptor agonists noradrenaline and clonidine modulated nitrergic neurotransmission in the guinea-pig basilar artery. 5. The findings show that ACh acts on prejunctional muscarinic receptors of nitrergic nerves to inhibit nitrergic neurotransmission. It is suggested that endogenous ACh may have this effect; however, the physiological significance of this prejunctional modulation is not clear due to the relatively small effect produced. The prejunctional inhibitory action of ACh may involve opening of neuronal K+ channels.
authors.affiliation: Department of Medical Laboratory Science, RMIT University, Melbourne, Victoria, Australia.
authors.forename: F
authors.initials: F
authors.lastname: Jiang
authors.forename: C G
authors.initials: CG
authors.lastname: Li
authors.forename: M J
authors.initials: MJ
authors.lastname: Rand
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology / Q000502:physiology*; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001315:Australia; D001488:Basilar Artery / Q000187:drug effects* / Q000294:innervation / Q000502:physiology; D015237:Dinoprost / Q000494:pharmacology; D004558:Electric Stimulation; D005260:Female; D006168:Guinea Pigs; D008297:Male; D026902:Potassium Channel Blockers; D015221:Potassium Channels / Q000187:drug effects; D011976:Receptors, Muscarinic / Q000187:drug effects; D009435:Synaptic Transmission / Q000187:drug effects* / Q000502:physiology; D014664:Vasodilation / Q000187:drug effects*; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D026902:Potassium Channel Blockers; D015221:Potassium Channels; D011976:Receptors, Muscarinic; D014665:Vasodilator Agents; D001285:Atropine; D015237:Dinoprost; D000109:Acetylcholine