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目的：研究内皮素（ET）、降钙素基因相关肽（CGRP）和钙离子（Ca2＋）对缺血再灌流所致肾损伤的影响及机理。方法：20只大耳白兔随机分成对照组和缺血再准流（IR）肾损伤组，观察肾缺血再池流24h时家兔肾组织中的ET、CGRP、Ca2＋含量和超微结构的变化。结果：IR组肾组织中的ET、CGRP、Ca2＋含量均较对照组显著升高（P＜0．05）；肾组织结构损伤较重。结论：缺血再泛流可刺激ET、CGRP和Ca2＋的产生和释放。ET可能通过强烈的缩血管作用，使缺血后产生无复流现象而致肾损伤；同时，ET通过多途径激活Ca2＋通道，Ca2＋大量内流，细胞内钙超载（CAO）而加重肾损伤；CGRP则可能通过拮抗ET缩血管和本身扩血管的效应而参与减轻肾损伤的作用。
Objective: To investigate the effects and mechanisms of endothelin (ET), calcitonin gene related peptide (CGRP) and calcium ion (Ca2 +) on renal injury induced by ischemia / reperfusion. Methods: Twenty rabbits were randomly divided into control group and IR group. The levels of ET, CGRP, Ca2 + and ultrastructure in kidneys of kidneys were observed after 24h of ischemia reperfusion. The change. Results: The contents of ET, CGRP and Ca2 + in renal tissue of IR group were significantly higher than those in control group (P <0.05). The renal tissue structure was more damaged. Conclusion: Ischemic re-flow can stimulate the production and release of ET, CGRP and Ca2 +. ET may cause renal damage by no-reflow phenomenon after ischemic injury through ET. In the meantime, ET activates Ca2 + channels through multiple channels, and massive influx of Ca2 + and intracellular calcium overload (CAO) aggravate renal injury. CGRP may be involved in reducing kidney damage by antagonizing the effects of ET vasoconstrictor and vasodilator itself.