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目的 探讨降钙素基因相关肽 (CGRP)对正常及模拟缺血缺氧状态下豚鼠心肌细胞钙通道电流的作用。方法 标准全细胞膜片钳记录方式。结果 当心室肌细胞由保持电压 - 40mV除极到 0mV时 ,10 -9、10 -8、和 10 -7mol·L-1的CGRP分别使正常状态下ICa L由 (1 2 6± 0 18)nA (n=8)增加到 (1 87± 0 2 5 )nA (P <0 0 5 ,n =8) ,(1 90±0 2 6 )nA (P <0 0 5 ,n =6 )和 (2 10± 0 2 7)nA (P <0 0 5 ,n=5 ) ;使模拟缺血缺氧状态下ICa L由原来的 (0 71± 0 10 )nA (n =8)增加到 (0 95± 0 12 )nA (P <0 0 1,n =6 ) ,(1 13± 0 15 )nA (P <0 0 5 ,n =4)和 (1 2 6± 0 13)nA(P <0 0 5 ,n =4) ,且对ICa L的最大激活电位无明显影响 ,两者差异无统计学意义。结论 CGRP对正常及模拟缺血缺氧状态下ICa L有明显的促进作用 ,该作用可能是CGRP发挥其心血管效应的离子通道机制之一。
Objective To investigate the effect of calcitonin gene related peptide (CGRP) on calcium channel currents in guinea pig cardiomyocytes under normal and hypoxia conditions. Methods Standard whole-cell patch-clamp recording method. RESULTS: When ventricular myocytes were depolarized to 0 mV from a holding voltage of 40 mV, CGRP at 10 -9, 10 -8, and 10 -7 mol·L -1 respectively increased ICa L from (122 ± 0 18) nA (n = 8) increased to (187 ± 025) nA (P <0 05, n = 8), (1 90 ± 0 2 6) nA (2 10 ± 0 2 7) nA (P <0 05, n = 5); the ICa L of simulated hypoxic-ischemic state was increased from 0 71 ± 0 10 nA (n = 8) to 0 95 ± 0 12) nA (P <0 0 1, n = 6), (1 13 ± 0 15) nA (P 0 05, n 4) and (12 6 ± 0 13) nA <0 0 5, n = 4), and had no significant effect on the maximum activation potential of ICa L, the difference was not statistically significant. Conclusion CGRP can significantly promote ICa L in normal and hypoxic-ischemic states, which may be one of the mechanisms of CGRP to exert its cardiovascular effects.