高血圧に因る動脈壁脂質水解酵素活性の変動

Abstract

In an attempt to investigate the mechanism by which hypertension accelerates atherosclerosis, fluctuation due to hypertension in aortic acid cholesteryl ester hydrolase (CEH), N-acetyl-β-glucosaminidase (NAGA) and acid phosphatase (AP) activities, were examined. SHRSP (stroke prone spontaneously hypertensive rats), SHR (spontaneously hypertensive rats) and WKR (normotensive Wistar Kyoto rats) were treated for 2 and 4 months with hypotensive drugs (reserpine, methyclothiazide and hydralazine); and arterial and venous enzyme activities were com- pared between the treated and nontreated rats. The results were also compared with those in DOCA-salt hypertension, which was induced by treating Wistar strain rats with DOCA (5mg/rats s. c. twice weekly for 1 month, 1% NaCl given as drinking water).In spontaneously hypertensive rats, blood pres-sure of SHRSP (219mmHg) and SHR (172mmHg) was lowered to almost normal levels due to the hypotensive treatment, which hardly affected the blood pressure of WKR. Acid CEH activity in the aorta from nontreated SHRSP and SHR was significantly lower than the activity in the treated SHRSP and SHR respectively. Reversely, aortic NAGA activity was higher in the former group. However, both the activities in the vein was not different between the two groups. No effect of the treatment was observed in WKR. Accompanying a decrease in the enzyme activity there was a significant increase in aortic cholesterol content in the nontreated groups compared to the treated ones; the percent increase in cholesteryl ester was 108% (SHRSP) and 95% (SHR), and that in free cholesterol was 43% (SHRSP) and 14% (SHR).In DOCA hypertensive rats, CEH and AP activities were significantly higher both in the aorta and the vein compared with those in the control rats. NaCl loading as drinking water also produced a similar result. These results indicate 1) that hypertension affected arterial CEH activity, leading to an accumulation of cholesterol, and 2) that an increase in CEH activity due to DOCA hypertension seemed ascribale to humoral factors.