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 mumol/L prostaglandin F2 alpha and a possible role of K+ channels in mediating the effects was investigated. 2. Acetylcholine (3 mmol/L) and physostigmine (10 mumol/L) produced small, yet statistically significant, inhibitions of EFS-induced nitrergic relaxations, while atropine (1 mumol/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 mumol/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 alpha 2-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.
journal_name
Clin Exp Pharmacol Physioljournal_title
Clinical and experimental pharmacology & physiologyauthors
Jiang F,Li CG,Rand MJkeywords:
subject
Has Abstractpub_date
1999-04-01 00:00:00pages
364-70issue
4eissn
0305-1870issn
1440-1681journal_volume
26pub_type
杂志文章abstract::1. Stroke is the second most common cause of death and a major cause of disability worldwide. Despite increasing knowledge of the cellular and molecular mechanisms that occur in stroke, there are still large gaps in our understanding that are impeding therapeutic progress. In addition, there are no drugs yet that can ...
journal_title:Clinical and experimental pharmacology & physiology
pub_type: 杂志文章,评审
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journal_title:Clinical and experimental pharmacology & physiology
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更新日期:1994-04-01 00:00:00
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更新日期:1991-07-01 00:00:00
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pub_type: 杂志文章
doi:10.1111/j.1440-1681.1983.tb00231.x
更新日期:1983-09-01 00:00:00
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更新日期:1995-08-01 00:00:00
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pub_type: 杂志文章
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更新日期:2000-03-01 00:00:00
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更新日期:1988-12-01 00:00:00
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journal_title:Clinical and experimental pharmacology & physiology
pub_type: 杂志文章,评审
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更新日期:1994-10-01 00:00:00