心钠素对神经肽Y刺激培养的血管平滑肌细胞蛋白合成的影响

为研究高血压时肽类神经激素与血管壁结构改变之关系，应用自发性高血压大鼠（SHR）及Wistar大鼠动脉平滑肌细胞（SMC）培养以及3H－胸腺嘧啶核苷、3H－亮氨酸掺入方法，观察到用神经肽Y（NPY）作用48h后可促进SHR离体培养的血管SMCDNA合成增加28．0％，蛋白会成增加54．6％（与血清对照组比较），而细胞数无明显增加。当同时加入心钠素（ANP）后，正常血压大鼠中DNA和蛋白合成分别下降42．3％和44．3％，而SHR中仅分别降低11．4％和10．6％。结果表明NPY可促进血管SMC肥大（蛋白含量增加40％即表明细胞肥大），ANP可拮抗NPY促细胞肥大效应，但在SHR中ANP对血管SMC的调节作用减弱是引起细胞肥大的重要原因之一。

Regulative Role of ANP in NPY-stimulated Protein Synthesis in Cultured Vascular Smooth Muscle Cells

To investigate the relationship between neuropeptide hormones and alterations of vascular structures in hypertension, we applied the method of cellular culture, tritiated thymidine and leucine incorpo-ration. We observed that 48-hour exposure to neuropeptide Y for these cells caused 28.0% and 54. 6 % in-creases respectively in DNA and protein synthesis (compared with serum control) as measured by tritiated TdR and leucine incorporation in cultured VSMC of SHR. But it did not accelerate an increase in cell number of SHR and Wistar rats. After exposure to both ANP and NPY in SMC of Wistar rats, DNA and protein synthesis contents were inhibited by 42. 3 % and 44. 3 % decreases, but in SHR, their contents were inhibit-ed by 11. 4 % and 10. 6 %. The results demonstrated that NPY accelerated VSMC hypertrophy whereas ANP prevented development of the hypertrophy in Wistar rats, but in SHR, ANP did not prevent SMC hy-pertrophy stimulated by NPY. The reductions in regulative effects of ANP on VSMC may play an important role in NPY-stimulated VSMC hypertrophy in SHR.