CORRELATIONS BETWEEN BLOOD PRESSURE AND BODY WEIGHT, SERUM LEPTIN IN HIGH CALORIE DIET-INDUCED OBESE RATS

Objective To examine the change of body weight （BW） and blood pressure （BP） in obese rats, clarify relationships between BP and BW and other factors. Methods Male Spraque-Dawley rats were fed either with normal diet （ND） or high calorie diet （HC） for 20 weeks. BW and BP of tail artery were observed biweekly and tetraweekly respectively; serum leptin and fasting insulin （FINS） were detected by enzyme-linked immunoadsordent assay （ELISA） and radioimmunoassay （RIA） respectively. Fasting plasma glucose （FPG） and free fatty acid（FFA） were measured by conventional means. Results BW, abdominal fat weight （AFW）, ratio of abdominal fat weight to body weight （RF/W）, systolic blood pressure （SBP）, diastolic blood pressure （DBP）, serum levels of leptin and FINS, FPG, FFA increased in the HD group after 20 weeks diet intervention （P〈0.05 or P〈0.01 ）. SBP was strongly correlated with BW, leptin, FINS and FFA （P〈0.05）, DBP was correlated with FFA （ r =0.47, P〈0.05）. In addition, leptin was positively correlated with BW, AFW, RF/W, FINS and FFA （P〈0.05 or P〈0.01 ）. Conclusion In this study of high calorie-diet induced rats, the gain of BW is accompanied by increased BP. The obese rats have hyperleptinemia, hyperinsulinemia, hyperglycemia and dyslipidemia which may have important effects on the development of obesityrelated hypertension. RF/W is the key factor in which affect serum leptin level.     

自发性高血压大鼠肠系膜动脉平滑肌细胞BKCa通道的活性及表达改变

目的 观察自发性高血压大鼠(spontaneous hypertensive rats, SHR)与Wistar-Kyoto(WKY)大鼠肠系膜动脉血管平滑肌细胞(vascular smooth muscle cells, VSMCs)大电导钙激活钾通道(large conductance calcium-activated potassium channel, BKCa)电流及通道α亚单位表达的差异.方法 实验采用16～18周龄SHR(N=20)及WKY(N=20)大鼠,尾套法测量大鼠尾动脉血压;胶原酶分离VSMCs,全细胞膜片钳技术记录全细胞总钾电流密度及BKCa电流;激光共聚焦观察BKCaα亚单位在VSMCs胞膜及胞质内的分布.结果 SHR较WKY大鼠的收缩压与舒张压均有显著升高(P<0.05);全细胞外向钾电流密度及BKCa电流密度均有显著性增加(P<0.05);SHR的BKCaα亚单位在胞膜及胞质内均有广泛分布,SHR大鼠VSMCs胞质与胞膜的荧光强度较WKY大鼠均有显著性升高(P<0.05).结论 BKCa电流密度增加可能与BKCa通道α亚单位的表达增多有关,SHR大鼠VSMCs的BKCa电流密度增加引起血管的舒张,不能抵消平滑肌细胞的肌源性收缩可能是导致高血压的发生机制之一.     

高脂饮食对血管平滑肌细胞KATP通道功能的影响

目的 观察高脂饮食对血管平滑肌的KATP通道功能的影响,探讨KATP通道在肥胖引起的可逆性高血压发病机制中的作用.方法 高脂饲料喂养大鼠,获得肥胖模型;20周后,其中10只转为普通饲料喂养,而另外10只继续喂养高脂饲料,实验继续10周.对照鼠为普通饲料喂养30周大鼠.30周时,处死大鼠,采用肌张力描记系统,膜片钳技术检测KATP通道的功能.结果 KATP通道电流及其介导的血管舒张反应在高脂鼠中明显降低,但转为普通饮食后,这些损伤被修复.结论 高脂饮食可引起大鼠血管平滑肌KATP通道功能的可逆性损伤,这可能是肥胖调节血压的一条潜在途径.