Rajashree S, Puvanakrishnan R
Department of Biotechnology, Central Leather Research Institute, Madras, India.
Mol Cell Biochem. 1999 Jul;197(1-2):203-8. doi: 10.1023/a:1006991009036.
This study was designed to investigate the alterations in the levels of various proteases such as angiotensin converting enzyme (ACE), kallikrein, aminopeptidases, urokinase and plasmin in serum-heart and kidney and to find out whether the changes in the levels of these enzymes could explain the pathogeneses of hypertension induced by Dexamethasone (Dex). Dex was administered to Male Wistar rats (180-200 g body weight) at a dosage of 2.5 mg/kg/week subcutaneously on alternate days for 2 weeks. One more week was included in this investigation to oversee the recovery process. Mean Arterial Pressure (MAP) showed significant elevation during administration and after withdrawal of Dex. The levels of enzymes such as angiotensin converting enzyme, carboxypeptidase-N and leucine aminopeptidase were found to be elevated in serum as well as in tissues. The level of kallikrein was observed to decrease in serum and tissues and that of thrombin, plasmin and urokinase exhibited variations. Thus, treatment with Dex altered the levels of these proteases which might have a role in the pathogenesis of hypertension and in altered blood coagulation.
本研究旨在调查血清、心脏和肾脏中各种蛋白酶水平的变化,如血管紧张素转换酶(ACE)、激肽释放酶、氨肽酶、尿激酶和纤溶酶,并探究这些酶水平的变化是否能解释地塞米松(Dex)诱导的高血压的发病机制。将雄性Wistar大鼠(体重180 - 200克)以2.5毫克/千克/周的剂量隔天皮下注射Dex,持续2周。本研究还包括另外一周以监测恢复过程。在给予Dex期间及停药后,平均动脉压(MAP)显著升高。发现血清和组织中血管紧张素转换酶、羧肽酶 - N和亮氨酸氨肽酶等酶的水平升高。观察到血清和组织中激肽释放酶水平降低,凝血酶、纤溶酶和尿激酶水平出现变化。因此,Dex治疗改变了这些蛋白酶的水平,这可能在高血压发病机制和凝血改变中起作用。