Desir Gary V
Department of Medicine, Yale University School of Medicine, New Haven, Connecticut 06520-8029, USA.
Curr Opin Nephrol Hypertens. 2008 Mar;17(2):181-5. doi: 10.1097/MNH.0b013e3282f521ba.
Recent experimental data shed light on the regulation of renalase, a secreted amine oxidase, which circulates in an inactive form (prorenalase). Abnormalities in the renalase pathway are evident not only in animal models of chronic kidney disease, but also during the development of hypertension, at a time when kidney function appears normal.
Prorenalase is rapidly (30-60 s) activated by increased plasma catecholamines and systolic blood pressure. Catecholamine administration promotes the secretion of preformed renalase within 5 min. Plasma renalase is markedly reduced in patients with chronic kidney disease and end-stage renal disease, and in animal models of chronic kidney disease and salt-dependent hypertension. Rats subjected to subtotal nephrectomy develop hypertension and chronic kidney disease, and exhibit low plasma and cardiac renalase, and abnormal renalase activation.
The renalase pathway is a previously unrecognized mechanism for regulating circulating catecholamines, cardiac function and blood pressure. In this pathway, prorenalase is rapidly activated by increased catecholamines and converted to renalase, which in turn degrades catecholamines. Abnormalities in the renalase pathway are evident in animal models of chronic kidney disease and hypertension. Collectively, these data suggest that renalase plays a key role in the regulation of sympathetic tone, blood pressure and cardiac function.
近期实验数据揭示了肾酶（一种分泌型胺氧化酶）的调节机制，它以无活性形式（前肾酶）循环。肾酶途径的异常不仅在慢性肾病动物模型中明显，而且在高血压发展过程中，即使肾功能看似正常时也很明显。
前肾酶可被血浆儿茶酚胺增加和收缩压迅速（30 - 60秒）激活。给予儿茶酚胺可在5分钟内促进预先形成的肾酶分泌。慢性肾病和终末期肾病患者以及慢性肾病和盐依赖性高血压动物模型中的血浆肾酶明显降低。接受肾次全切除术的大鼠会发展为高血压和慢性肾病，并表现出血浆和心脏肾酶水平低以及肾酶激活异常。
肾酶途径是一种以前未被认识的调节循环儿茶酚胺、心脏功能和血压的机制。在该途径中，前肾酶被增加的儿茶酚胺迅速激活并转化为肾酶，肾酶进而降解儿茶酚胺。肾酶途径的异常在慢性肾病和高血压动物模型中很明显。总体而言，这些数据表明肾酶在调节交感神经张力、血压和心脏功能中起关键作用。
