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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。
PURPOSE AND METHODS: Patch clamp whole cell recording was used to observe the effect of VNP on L-type calcium channel current (ICa, L) in isolated rat ventricular myocytes. Results: When ventricular myocytes were depolarized to 0mV by holding voltage 40mV, the peak currents of ICa and L were reduced by 31.05% and 46.95% respectively at VNP of 0.1, 0.2 and 0.4μmol / L, And 60.75%. The inhibition was not related to the rundown phenomenon of ICa, L, and had no significant effect on the maximum activation potential of ICa, L. When ICa, L was pre-activated by isoprenaline (10-7mol / L), VNP (0.2μmol / L) still decreased the peak current of ICa, L by 18.23%. CONCLUSION: VNP has a definite inhibitory effect on ICa and L of rat ventricular myocytes, and this effect may be one of the ion channel mechanisms by which VNP exerts its cardiovascular effect.