The effects of acetylcholine and dopamine on carotid chemosensory activity in the rabbit.
The effects of acetylcholine and dopamine on carotid chemosensory activity in the rabbit.
复制标题
乙酰胆碱和多巴胺对兔颈动脉化学感应活性的影响。
DOI：
10.1113/jphysiol.1979.sp012704
复制
发表时间：
1979
期刊：
影响因子：
--
通讯作者：
D. McQueen
中科院分区：
文献类型：
--
作者：
R. Docherty;D. McQueen
1.颈动脉内（I.C.）注射乙酰胆碱（ACh）或多巴胺可抑制麻醉家兔窦神经外周切断端记录到的自发化学感受活动。2.高剂量乙酰胆碱（大于或等于50微克I.C.）诱发轻微增加放电之前的抑制。这种兴奋归因于药物的烟碱作用，因为它被美加明消除。3.毒蕈碱激动剂氨甲酰胆碱抑制化学感受器活性，这种作用被高剂量阿托品阻断，因为ACh引起的抑制作用也是如此。多巴胺诱导的抑制不受阿托品的影响。4.阿托品，在剂量足以取消ACh的血管抑制作用，只有轻微减少ACh对化学感受器的抑制作用。此外，血管扩张剂亚硝酸钠和硝普钠没有明显改变化学感觉放电。因此，对ACh的抑制反应不太可能继发于血管变化。5.多巴胺拮抗剂α-氟哌噻吨可阻断对多巴胺的抑制反应，但对乙酰胆碱的抑制反应不受影响。这意味着抑制化学感受活性诱发的外源性乙酰胆碱不是继发于多巴胺的释放。6.结果的影响进行了讨论，特别是关于可能的生理作用的乙酰胆碱作为调制器的颈动脉化学感受活动。
1. Intracarotid (I.C.) injection of either acetylcholine (ACh) or dopamine inhibited spontaneous chemosensory activity recorded from the peripheral cut end of the sinus nerve in the anaesthetized rabbit. 2. High doses of ACh (greater than or equal to 50 micrograms I.C.) evoked a slight increase in discharge which preceded the inhibition. This excitation was attributable to a nicotinic action of the drug since it was abolished by mecamylamine. 3. The muscarinic agonist bethanechol inhibited chemoreceptor activity, an effect which was blocked by high doses of atropine, as was the inhibition caused by ACh. Dopamine‐induced inhibition was unaffected by atropine. 4. Atropine, in doses sufficient to abolish the vasodepressor effect of ACh, only slightly reduced the inhibitory action of ACh on the chemoreceptors. Also, the vasodilators sodium nitrite and sodium nitroprusside did not appreciably alter chemosensory discharge. It seems unlikely, therefore, that the inhibitory response to ACh is secondary to vascular changes. 5. The inhibitory response to dopamine, but not that to ACh, was blocked by the dopamine antagonist alpha‐flupenthixol. This implies that inhibition of chemosensory activity evoked by exogenous ACh was not secondary to dopamine release. 6. The implications of the results are discussed, particularly with regard to the possible physiological role of ACh as a modulator of carotid chemosensory activity.