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作 者:张翀[1] 朱汉威[1] 蒋更如[1] 刘秀英[1]
机构地区:[1]上海第二医科大学新华医院肾脏内科,上海200092
出 处:《肾脏病与透析肾移植杂志》2003年第4期340-343,共4页Chinese Journal of Nephrology,Dialysis & Transplantation
摘 要:目的 :研究血管紧张素Ⅱ (AngⅡ )和血小板衍生生长因子BB(platelet derivedgrowthfactor BB ,PDGF BB)引起的肾小球系膜细胞 (MC)内游离钙浓度变化的异同。 方法 :以体外培养的MC为研究对象 ,激光共聚焦显微术结合Fura 3染色法动态测定细胞内游离钙浓度。 结果 :AngⅡ和PDGF BB均可浓度依赖性地引起MC内游离钙浓度的升高 ,但二者的动态变化曲线存在显著不同。无钙缓冲液和钙通道阻滞剂均可抑制AngⅡ和PDGF BB引起的细胞内钙浓度变化 ,但其抑制的方式和程度均有所不同。 结论 :AngⅡ和PDGF BB通过不同的激发途径引起MC内游离钙浓度的升高。Objective:To investigate the intracellular calcium concentration ([Ca 2+] I) alteration induced by Angiotensin Ⅱ(Ang Ⅱ) and platelet derived growth factor (PDGF)-BB in cultured glomerular mesangial cells. Methodology:Rat mesangial cells were cultured. [Ca 2+] I was detected using fluorescentprobe fluo-3/AM and a laser scanning confocal microscope. Results:Both AngⅡ and PDGF-BB significantly increased [Ca 2+] i in a dose-dependent manner, but the temporal pattern and magnitude of the calcium responses were significantly different. AngⅡ-induced elevation in [Ca 2+] i was biphasic. In the initial phase, namely the peak response, [Ca 2+] i increased seven- to eight-fold above baseline, and then rapidly declined to sustained level. However, PDGF-BB-induced was relatively slow, and the peak concentrations were only approximately two-fold above baseline. Correspondence to this, the decline of [Ca 2+] i was also slow, and [Ca 2+] i still higher above baseline till 200 second later. The Ca 2+-free bath and calcium channel blocker nifedipine inhibited the elevation in [Ca 2+] i induced by both AngⅡ and PDGF-BB, but the temporal pattern and magnitude of the inhibitory effect on AngⅡ and PDGF-BB were also significantly different. Conclusion:Ang Ⅱ and PDGF-BB induce [Ca 2+] i elevation in cultured mesangial cells by the different pathways.
关 键 词:血管紧张素Ⅱ 血小板衍生生长因子BB 游离钙 肾小球系膜细胞 测定 硝苯地平
分 类 号:R33[医药卫生—人体生理学]
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