Song S, Yim K W, Kim N Y, Yoon B C, Lee D H, Jung H C, Kim C Y
Department of Internal Medicine, Seoul National University College of Medicine, Korea.
Korean J Intern Med. 1994 Jul;9(2):67-71. doi: 10.3904/kjim.1994.9.2.67.
Angiotensin converting enzyme (ACE) has been shown to be an important peptidasse that play a role in digestion and assimilation of protein rich in proline such as casein, gliadin and collagen. Despite that ACE inhibitors have been popular for various types of hypertension and congestive heart failure, the effects of their long-term treatment on intestinal ACE activities are not known. Therefore, we measured intestinal specific activities in rats after four weeks' treatment of ACE inhibitors.
Thirty Wistar rats weighing about 200g in average were divided into three groups, and supplied with tap water, captopril solution and enalapril solution respectively for four weeks. After sacrificing, intestinal ACE specific activities were measured in homogenate and brush border membrane fraction respectively, which was prepared from three equally divided segments of removed small intestine.
ACE specific activities of proximal, middle and distal segments of control group were 178.6 +/- 64.2, 180.3 +/- 60.2 and 48.6 +/- 13.1 in brush border membrane (mean +/- SD, nmol/min/mg protein) respectively. Those of captopril group were 314.2 +/- 72.5, 281.0 +/- 69.8 and 67.7 +/- 21.8 respectively, showing tendency of increase in proximal and middle segments (p < 0.01 and 0.05 respectively). By contrast, those of enalapril group were 48.5 +/- 27.6, 70.7 +/- 15.6 and 11.6 +/- 4.4 respectively, which were significantly lower (p < 0.01) than those of control group.
Rat intestinal ACE specific activities were not inhibited by captopril treatment, but inhibited by enalapril treatment. This finding may explain why there has not been any case report of malabsorption in patients taking captopril. But the malabsorption of prolyl peptide could be possible in cases with long-term administration of enalapril.
血管紧张素转换酶（ACE）已被证明是一种重要的肽酶，在富含脯氨酸的蛋白质（如酪蛋白、麦醇溶蛋白和胶原蛋白）的消化和吸收中发挥作用。尽管ACE抑制剂已广泛应用于各种类型的高血压和充血性心力衰竭，但其长期治疗对肠道ACE活性的影响尚不清楚。因此，我们在大鼠接受四周ACE抑制剂治疗后测量了肠道特异性活性。
将30只平均体重约200g的Wistar大鼠分为三组，分别给予自来水、卡托普利溶液和依那普利溶液四周。处死后，分别在匀浆和刷状缘膜部分测量肠道ACE特异性活性，这些部分由取出的小肠等分为三段制备而成。
对照组近端、中段和远端刷状缘膜的ACE特异性活性分别为178.6±64.2、180.3±60.2和48.6±13.1（平均±标准差，nmol/分钟/毫克蛋白）。卡托普利组分别为314.2±72.5、281.0±69.8和67.7±21.8，近端和中段呈升高趋势（分别为p<0.01和0.05）。相比之下，依那普利组分别为48.5±27.6、70.7±15.6和11.6±4.4，显著低于对照组（p<0.01）。
卡托普利治疗未抑制大鼠肠道ACE特异性活性，但依那普利治疗可抑制。这一发现可能解释了为何尚无服用卡托普利患者出现吸收不良的病例报告。但长期服用依那普利的情况下，脯氨酰肽的吸收不良可能会发生。
