摘要
通过测定培养的心肌细胞~3H-leucine(~3H-亮氨酸)掺入率和膜片钳全细胞记录方法记录Ca^(2+)电流(I_(ca)),研究神经肽Y(NPY)、维拉帕米对大鼠心肌细胞肥大的影响。结果:0.1μmol/L NPY促使培养的心肌细胞~3H-leucine掺入率增大,达(136.0±4.4)min^(-1),与对照组(91.0±4.O)min^(-1)相比,差异有显著性意义(p<0.01)。10nmol/L维拉帕米与NPY共同作用于心肌细胞24h,可使NPY促~3H-leucine掺入率增大的作用受到抑制(P<0.01)。NPY可显著增大心肌细胞I_(ca),为(12.0±3.1)pA,与对照组(5.5±2.4)pA比较,差异有显著性意义(P<0.01)。结论:NPY促使培养的心肌细胞蛋白质合成率增大的作用可被维拉帕米阻断,而NPY增加细胞内游离钙,触发心肌蛋白质合成增加,可能是促进心肌肥大的机制之一。
In order to study the effect of neuropeptide Y (NPY).verapamil on cardiomyocyte hypertrophy, the patch clamp technique was employed to detect the current density of calcium channel and 3H-leucine in-corporation. 0. 1 mol/L NPY could increase the cultured myocyte 3 H-leucine incotpotation up to (136. 0i 4.4) min,with the difference being significant (P<0. 01) as compared with the control (91. 0?. 0) min. Under the same condition,10 nmol/L verapamil and NPY were incubated together with myocytes for 24 h, the NPY-promoted increase of 3H-lecucine incorporation was inhibited (P><0. 01 ). The myocyte cur-rent was obviously increased by NPY to (12. 0?. 1) pA as compared with the control (5. 5?. 4) pA (P< 0.01). It was concluded that NPY could stimulate the protein synthesis of the cultured myocytes, which could be antagonized by verapamil. NPY could increase the calcium current and trigger the myocyte protein synthesis,which might be one of the mechanisms of myocardium hypertrophy.
出处
《同济医科大学学报》
CSCD
1998年第5期382-384,共3页
Acta Universitatis Medicinae Tongji
基金
国家自然科学基金资助项目(No.39070408)
