Wang Y, Baimbridge K G, Mathers D A
Department of Physiology, University of British Columbia, Vancouver, Canada.
Can J Physiol Pharmacol. 1991 Mar;69(3):393-9. doi: 10.1139/y91-060.
Smooth muscle cells were dissociated from conducting cerebral arteries of adult rats and maintained in culture for 2-4 days. The calcium-sensitive fluorescent probe, fura-2, was used to study the effect of the vasoconstrictor serotonin (5-HT) on the level of free intracellular Ca2+ in these cells. The baseline level of free intracellular calcium was 39 +/- 3.6 nM. In 74 out of 110 cells, 5-HT application transiently increased the free Ca2+ content. This effect was dose-dependent and was suppressed by nanomolar concentrations of the 5-HT2 receptor antagonist, ketanserin. The 5-HT induced rise in free intracellular calcium was not prevented by the presence of Co2+, La3+, or nifedipine, blockers of voltage-sensitive calcium channels. These results indicate that 5-HT mobilizes intracellular Ca2+ in cultured smooth muscle cells derived from the rat cerebrovasculature. The mobilization of intracellular Ca2+ appears to be triggered by a 5-HT2 type receptor, although further pharmacological experiments are required to verify this hypothesis.
从成年大鼠的大脑传导动脉中分离出平滑肌细胞,并在培养中维持2 - 4天。使用钙敏感荧光探针fura - 2来研究血管收缩剂血清素(5 - HT)对这些细胞内游离Ca2+水平的影响。细胞内游离钙的基线水平为39±3.6 nM。在110个细胞中的74个细胞中,应用5 - HT可使游离Ca2+含量短暂增加。这种效应是剂量依赖性的,并被纳摩尔浓度的5 - HT2受体拮抗剂酮色林所抑制。5 - HT诱导的细胞内游离钙升高不受电压敏感性钙通道阻滞剂Co2+、La3+或硝苯地平的存在的阻止。这些结果表明,5 - HT可动员源自大鼠脑血管系统的培养平滑肌细胞内的Ca2+。细胞内Ca2+的动员似乎是由5 - HT2型受体触发的,尽管需要进一步的药理学实验来验证这一假设。