血管紧张素Ⅱ受体1型
血管紧张素II
内科学
内分泌学
细胞凋亡
肾
受体
血管紧张素受体
标记法
肾素-血管紧张素系统
平衡
医学
化学
生物
免疫组织化学
血压
生物化学
作者
Marzenna Podhorska‐Okołów,Piotr Dzięgiel,Agnieszka Gomułkiewicz,Barbara Dolińska-Krajewska,Eugenia Murawska‐Ciałowicz,Z Jethon,M. Zabel
出处
期刊:PubMed
日期:2004-01-01
卷期号:49 Suppl 1: 8-10
被引量:10
摘要
Intensive physical exercise disturbs the entire homeostasis in the body and leads to changes in haemodynamic and metabolic alterations not only in skeletal muscles but also in many distant organs. In response to acute physical exercise, a decrease of the glomerular filtration may occur, followed by stimulation of the renin-angiotensin system (RAS). Recent studies have shown that both AT1 and AT2 angiotensin receptors may play a role in mediating the apoptotic process in the kidney. Our previous studies have demonstrated an occurrence of apoptosis in rat renal tubular cells after an excessive exercise. The aim of the present study was to determine the possible mechanism of exercise-induced apoptosis in rat kidney. The analysis was performed on kidneys of rats, subjected to treadmill running until exhaustion. Apoptosis was detected in paraffin sections by the TUNEL technique. The expression of AT1 and AT2 receptors in renal tubular cells was examined by immunohistochemistry and Western blot. Our results confirmed that apoptosis after physical exercise is present in renal distal tubular cells. Moreover, there was an increased expression of AT1 and AT2 receptors in distal tubular cells. These studies suggest that physical exercise may induce apoptosis by a mechanism, involving the activation of angiotensin AT1 and AT2 receptors.
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