Erdbrügger W, Vischer P, Bauch H J, Michel M C
Institute for Arteriosclerosis Research, University of Münster, Germany.
J Cardiovasc Pharmacol. 1993 Jul;22(1):97-102. doi: 10.1097/00005344-199307000-00016.
We used the fluorescent Ca2+ indicator Fura-2 in cultured porcine aortic smooth muscle cells (PASMC) to study effects of the sympathetic neurotransmitters norepinephrine (NE) and neuropeptide Y (NPY) on free intracellular Ca2+ (Cai). Both transmitters transiently increased intracellular Ca2+ in a concentration-dependent manner. Selective agonists and antagonists demonstrated that the NE-stimulated Cai increase is predominantly (if not exclusively) mediated by alpha 2-adrenoceptors, whereas the NPY response appears to be mediated by the peptide YY-insensitive Y3-like receptor subtype. Pretreatment of cells with pertussis toxin abolished NPY and alpha-adrenoceptor agonist-stimulated intracellular Ca2+ elevations (but not those stimulated by angiotensin II) suggesting involvement of a Gi-like G-protein. alpha 2-Adrenoceptor-stimulated Ca2+ increases resulted from mobilization from intracellular stores, whereas Y3-like NPY receptors mobilized Ca2+ from intracellular stores and also promoted Ca2+ influx.
我们在培养的猪主动脉平滑肌细胞(PASMC)中使用荧光Ca2+指示剂Fura-2,以研究交感神经递质去甲肾上腺素(NE)和神经肽Y(NPY)对细胞内游离Ca2+(Cai)的影响。两种递质均以浓度依赖的方式短暂增加细胞内Ca2+。选择性激动剂和拮抗剂表明,NE刺激引起的Cai增加主要(如果不是唯一)由α2-肾上腺素能受体介导,而NPY反应似乎由对肽YY不敏感的Y3样受体亚型介导。用百日咳毒素预处理细胞可消除NPY和α-肾上腺素能受体激动剂刺激引起的细胞内Ca2+升高(但不消除血管紧张素II刺激引起的升高),提示涉及一种Gi样G蛋白。α2-肾上腺素能受体刺激引起的Ca2+增加是由于细胞内储存库的动员,而Y3样NPY受体则从细胞内储存库动员Ca2+,并促进Ca2+内流。