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作 者:程树亮[1] 牛国保[1] 王跃民[1] 冯华松[1] 裴建明[1]
机构地区:[1]第四军医大学基础部生理教研室
出 处:《中国应用生理学杂志》1999年第2期107-110,共4页Chinese Journal of Applied Physiology
基 金:国家自然科学基金
摘 要:目的和方法:采用膜片钳全细胞记录方式观察血管钠素肽(VNP)对大鼠单个心室肌细胞L型钙通道电流(ICa,L)的影响。结果:当心室肌细胞由保持电压40mV除极到0mV时,0.1,0.2和0.4μmol/L的VNP分别使ICa,L内向电流峰值降低31.05%,46.95%和60.75%。该抑制作用与ICa,L的rundown现象无关,且对ICa,L的最大激活电位无明显影响。当ICa,L被异丙肾上腺素(10-7mol/L)预先激活后,VNP(0.2μmol/L)仍可使ICa,L电流峰值下降18.23%。结论:VNP对大鼠心室肌细胞ICa,L具有明确的抑制作用,该作用可能是VNP发挥其心血管效应的离子通道机制之一。Aim and Methods: The effect of external application of vasonatrin peptide (VNP) on L type calcium current (T Ca,L ) was stu died in single cells isolated from rat ventricle using the whole cell patch clamp technique.Results: It was found that 0.1, 0. 2 and 0.4 μmol/L VNP reduced I Ca,L peak currernt by an average of 31. 05%, 46. 95%,60. 75% respectively when the ventricular myocytes were depolarized to 0 mV from the holding potential ( 40 mV). This inhibitory effect of VNP on I Ca,L had no relation with the“rundown”phenomenon and little effect on the maxium activing potential of I Ca,L . When I Ca,L was increased by isoprenaline (10 -7 mol/L) preferentially, VNP (0. 2 μmol/L) could still decrease I Ca,L peak current by 18. 23%.Conclusion: These results indicate that VNP do have inhibitory effect on I Ca,L and this effect might be one of the mechanisms by which VNP regulates cardiovascular system. 〖HS1*2]
分 类 号:R331.38[医药卫生—人体生理学] Q516[医药卫生—基础医学]
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