非肥胖高血压病患者糖耐量与膜Ca^(2+)—ATP酶的变化

测定了40例非肥胖高血压病患者(NEH)及40例正常人的血糖、血清胰岛素、血脂及外周血红细胞膜基础Ca^(2+)-ATP酶活性.NEH组用卡托普利治疗4周.结果表明NEH胰岛和素释放试验各时限血清胰岛素浓度均显著增高,与血压呈正相关.血清甘油三脂明显增高,与空腹血清胰岛素浓度呈正相关.膜基础Ca^(2+)ATP酶活性显著下降,与空腹血胰岛素浓度、舒张压及平均动脉压呈负相关.卡托普利治疗后,血压显著下降,血清胰岛素浓度显著下降,膜基础Ca^(2+)-ATP酶活性增高.说明NEH存在糖耐受不良及膜基础Ca^(2+)-ATP酶活性的变化,高胰岛素血症与血压升高及该酶活性下降有关,卡托普利可逆转这些异常变比.

Blood glucose,serum insulin,lipid and peripheral basal erythrocyte caicium adenosine triphosphataseactivity were tested in 40 no ?obese patients with hypertension(NEH)and 40 nonnal subjects.The effects of Captopril on the NEH were observed during this study.The results showed that the concentrations of serum insulin and triglyceride in NEH increased significantly during the oral glucose tolerance tests and had positive correlation with blood pressure and the concentration of serum insulin in fasting, respectively. The basal erythrocyte calcium adnosine triphosphatase activity decreased singnificantly and had a negative correlation with the concentration of serum insulin in fasting,diastolic blood pressure and mean arterial pressure. Administered Captopril for 4 weeks, NEH had a decrease in blood prdssure and the concentration of serum insulin , but an increase in the basal erythrocyte calcium adnosine triphosphatase activity.