Shaw K, Montague W, Pallot D J
Department of Biochemistry, University of Leicester School of Medicine, U.K.
Biochim Biophys Acta. 1989 Sep 4;1013(1):42-6. doi: 10.1016/0167-4889(89)90125-0.
The effects of hypoxia and carbachol on the release of newly synthesized catecholamines from superfused rat carotid bodies have been examined. Hypoxic superfusion medium was found to evoke catecholamine release which was dependent on the extracellular calcium concentration and was reduced by nitrendipine and atropine. Superfusion with the muscarinic agonist, carbachol, stimulated catecholamine release independently of the oxygen tension of the medium. The effect of carbachol on catecholamine release was abolished by atropine, suggesting that it was mediated by activation of cholinergic receptors of the muscarinic type. Both hypoxia and carbachol stimulated the release of 45Ca from carotid bodies prelabelled with 45Ca. The release of 45Ca with either stimulus was reduced by atropine and nitrendipine. These results suggest that although extracellular calcium plays an important role in the exocytotic secretory process of the carotid body, the mobilization of intracellular calcium pools may also contribute to the secretory response.
研究了缺氧和卡巴胆碱对灌流大鼠颈动脉体新合成儿茶酚胺释放的影响。发现缺氧灌流液可引起儿茶酚胺释放,该释放依赖于细胞外钙浓度,并被尼群地平和阿托品所抑制。用毒蕈碱激动剂卡巴胆碱灌流可刺激儿茶酚胺释放,且与灌流液的氧张力无关。阿托品可消除卡巴胆碱对儿茶酚胺释放的影响,提示其作用是由毒蕈碱型胆碱能受体激活介导的。缺氧和卡巴胆碱均刺激预先用45Ca标记的颈动脉体释放45Ca。阿托品和尼群地平均可减少两种刺激下45Ca的释放。这些结果表明,尽管细胞外钙在颈动脉体的胞吐分泌过程中起重要作用,但细胞内钙库的动员也可能有助于分泌反应。