钙离子拮抗剂治疗高血压病患者过程中细胞内外钙调素水平的变化

THE CHANGE OF LEVEL OF INTRACELLULAR AND EXTRACELLULAR CALMODUL IN THE PROCESS OF CALCIUM ANTAGONISTS TREATING HYPERTENSIVE PATIENTS

从分子水平研究钙离子拮抗剂治疗高血压病的机制。用反转录聚合酶链反应法测定淋巴细胞内钙调素（ＣａＭ）基因的ｍＲＮＡ转录水平以及用ＲＩＡ法测定细胞外（即血清）ＣａＭ浓度，借以观察在用钙离子拮抗剂治疗高血压的过程中，细胞内外ＣａＭ水平的改变。发现随着正规服用钙拮抗剂治疗时间的延长，高血压患者淋巴细胞内ＣａＭ基因ｍＲＮＡ的转录水平亦受到抑制。服用钙拮抗剂时间长于３个月者，ｍＲＮＡ的转录水平显著降低（Ｐ＜０．０１），而治疗时间在１个月之内者，ＣａＭ基因的转录水平无明显变化（Ｐ＞０．０５）。对于细胞外ＣａＭ的水平，在服用钙拮抗剂治疗时间＜１个月者，血清ＣａＭ浓度下降，而长期服用钙拮抗剂的患者则相对增高，但均无统计学意义（Ｐ＞０．０５）。在用钙拮抗剂治疗高血压的过程中，细胞内和细胞外ＣａＭ的水平均发生变化。用钙离子拮抗剂治疗高血压病长于３个月者，细胞内ＣａＭ基因的ｍＲＮＡ转录水平明显受到抑制，而细胞外ＣａＭ浓度则无论服用钙离子拮抗剂时间长短。

To study the mechanism of action of calcium antagonists in the duration in hypertension therapy on the molecular level.Intracellular level of mRNA expression of CaM gene in lymphocyte was measured by the reverse transcript polymerease chain reaction analysis and extracellular level of calmodulin was measured by radioimmunology analysis to understand the change of CaM content in the duration with calcium antagonists therapy.The longer the hypertensive patients were treated by calcium antagonists,the less the mRNA of CaM gene was expressed.The intracellular level of CaM expession was decreased significantly in the patients who have been treated by calcium antagonists for more than 3 months ( P <0.01) while it did not change significantly in those patients who have been treated by calcium antagonists for less than 1 month ( P >0.05).As to the extracellular CaM content,we found it did not change significantly in the patients who have been treated by CaA for less than 1 month or more than 3 months( P >0.05).The level of intracellular and extracellular CaM changed in the patients with calcium antagonists therapy.intracellular CaM change indicated that the mRNA expression of CaM gene was suppressed significantly when the hypertensive patietns have been treated by CaA for more than 3 months while extracellular CaM content did not change obviously.Calcium and its intrecellular messanger transduction system are assumed to play an improtant role in the mechanism of hypertension from another study angle.