氨氯地平对自发性高血压大鼠血管平滑肌细胞生长的影响

本文采用自发性高血压大鼠（ＳＨＲ）动脉平滑肌细胞培养，３Ｈ－胸腺嘧啶核苷（３Ｈ－ＴｄＲ）和３Ｈ－亮氨酸（３Ｈ－Ｌｅｕｃｉｎｅ）掺入方法，观察到用氨氯地平（Ａｍｌｏｄｉｐｉｎｅ）作用４８小时后，与神经肽Ｙ（ＮＰＹ）组比较，其离体培养的ＳＨＲ动脉平滑肌细胞３Ｈ－ＴｄＲ掺入量降低５０．５％，３Ｈ－Ｌｅｕｃｉｎｅ掺入量降低５６．５％。氨氯地平组与对照组比较其３Ｈ－ＴｄＲ和３Ｈ－Ｌｅｕｃｉｎｅ掺入量分别降低５７．６％和３２．３％。用ＮＰＹ作用２４小时后，与对照组比较动脉平滑肌细胞３Ｈ－ＴｄＲ和３Ｈ－Ｌｅｕｃｉｎｅ掺入量却分别增加２０％和５４．６％。而细胞计数均无显著性差异（Ｐ＞０．０５）。结果表明，氨氯地平能有效地抑制ＳＨＲ血管平滑肌细胞（ＶＳＭＣ）的ＤＮＡ和蛋白质合成，以及显著的抑制ＮＰＹ引起的ＶＳＭＣ的ＤＮＡ合成和蛋白质合成增加效应。提示氨氯地平在阻遏高血压致心血管壁肥厚的发生发展中起着不容忽视的作用

THE EFFECT OF AMLODIPINE AND NEUROPEPTIDE Y IN MULTIPLICATION OF CULTURED ARTERIAL SMOOTH MUSCLE CELLS OF SPONTANEOUSLY HYPERTENSIVE RATS

Adding 3H Leucine in cultured arterial smooth muscle cells of spontaneously hypertensive rats(SHR), we have compared the Amoldipinlgroup compared with Neuropeptide Y(NPY) group. 48 hours after being given Amlodipine, the mixed amount of 3H TdR in cultured arterial smooth musle cells of SHR reduced to 50 5% and that of 3H Leucine reduced to 56 5%. Compared with the contul group, the mixed amount of 3H TdR and 3H Leucine reduced to 57 6% and 32 3% respectively. 24 hours after being given NPY. the mixed amout of 3H TdR and 3H Leucine increased by 20% and 54 6% respectively. However, the number of arterial smooth muscle cells in three groups had no obvious discrepancy(<0 05). The results showed that Amlodipine could effectively inhibit the increaseing synthesis of DNA and protein caused by NPY in vascular smooth muscle cells of SHR. In suggested that Amlodipin played a considerable role in inhibiting development and advancement of hypertrophy of cardiovascular wall initiated by hypertension.