Huang Y, Rogers J, Henderson G
Department of Pharmacology, University of Cambridge, England.
J Neurochem. 1987 Nov;49(5):1541-9. doi: 10.1111/j.1471-4159.1987.tb01025.x.
Angiotensin II (ANGII) (3-100 nM) facilitated the potassium-evoked (22.5 mM) release of [3H]-noradrenaline ([3H]NA) from slices of parietal cortex in a concentration-dependent manner, but did not significantly alter the release of [3H]NA evoked in a similar manner from locus coeruleus slices. The facilitatory action of ANGII was blocked by saralasin (0.1-3 microM). Neither nimodipine (10-30 microM) nor phenylmethylsulphonyl fluoride (1 mM) altered either [3H]NA release or the facilitatory action of ANGII in the parietal cortex. Carbachol (0.01-3 mM) and raised potassium (22.5 mM), but not ANGII (3-100 nM), stimulated the production of inositol phosphates in parietal cortex slices. The potassium-evoked increase in inositol phosphate production was unaffected by ANGII (3-100 nM). In the locus coeruleus, ANGII (3-100 nM) did not stimulate inositol phosphate production. The mechanism underlying the ANGII facilitation of [3H]NA release from the parietal cortex does not appear to involve either nimodipine-sensitive calcium channels, or, as far as we have been able to determine, the release of calcium from intracellular stores following the breakdown of phosphoinositides.
血管紧张素II（ANGII）（3 - 100 nM）以浓度依赖性方式促进顶叶皮质切片中钾离子诱发（22.5 mM）的[3H] - 去甲肾上腺素（[3H]NA）释放，但对蓝斑核切片中以类似方式诱发的[3H]NA释放无显著影响。ANGII的促进作用被沙拉新（0.1 - 3 microM）阻断。尼莫地平（10 - 30 microM）和苯甲基磺酰氟（1 mM）均未改变顶叶皮质中[3H]NA的释放或ANGII的促进作用。卡巴胆碱（0.01 - 3 mM）和升高的钾离子（22.5 mM）可刺激顶叶皮质切片中肌醇磷酸的生成，但ANGII（3 - 100 nM）无此作用。钾离子诱发的肌醇磷酸生成增加不受ANGII（3 - 100 nM）影响。在蓝斑核中，ANGII（3 - 100 nM）不刺激肌醇磷酸生成。ANGII促进顶叶皮质释放[3H]NA的机制似乎既不涉及对尼莫地平敏感的钙通道，就我们所能确定的而言，也不涉及磷酸肌醇分解后细胞内钙库的钙释放。
