Bialecki R A, Izzo N J, Colucci W S
Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.
Biochem Biophys Res Commun. 1989 Oct 16;164(1):474-9. doi: 10.1016/0006-291x(89)91744-0.
Conflicting evidence has been reported regarding the role of endothelin-1, a potent vasconstrictor peptide, in stimulating extracellular calcium influx in rabbit vascular smooth muscle. The objective of this study was to elucidate the effects of endothelin-1 on transmembrane 45Ca2+ influx and intracellular calcium mobilization in cultured rabbit aortic smooth muscle cells. In calcium containing buffer, endothelin-1 induced a concentration-dependent 45Ca2+ efflux response over the range of 10 pM to 100 nM with an EC50 of approximately 60 pM. Maximum endothelin-stimulated 45Ca2+ efflux was not affected by the absence of extracellular calcium or the presence of 1 microM verapamil. Endothelin-1 did not induce transplasmalemmal 45Ca2+ uptake at times up to 30 min. These findings suggest that an alteration in intracellular calcium handling, rather than extracellular calcium influx, is responsible for the endothelin-stimulated increase in intracellular calcium concentration in rabbit aortic smooth muscle cells.
关于强效血管收缩肽内皮素-1在刺激兔血管平滑肌细胞外钙内流中的作用,已有相互矛盾的证据报道。本研究的目的是阐明内皮素-1对培养的兔主动脉平滑肌细胞跨膜45Ca2+内流和细胞内钙动员的影响。在含钙缓冲液中,内皮素-1在10 pM至100 nM范围内诱导浓度依赖性的45Ca2+外流反应,EC50约为60 pM。最大内皮素刺激的45Ca2+外流不受细胞外钙缺失或1 microM维拉帕米存在的影响。内皮素-1在长达30分钟的时间内未诱导跨膜45Ca2+摄取。这些发现表明,细胞内钙处理的改变而非细胞外钙内流,是内皮素刺激兔主动脉平滑肌细胞内钙浓度升高的原因。