Exercise-induced apoptosis in rat kidney is mediated by both angiotensin II AT1 and AT2 receptors

Marzena Podhorska-Okolow, P. Dziegiel, A. Gomulkiewicz, D. Kisiela, B. Dolinska-Krajewska, Z. Jethon, U. Carraro, M. Zabel

Research output: Contribution to journalArticlepeer-review

Abstract

Excessive physical exercise may lead to disturbance of the entire homeostasis in the body, including damage not only in skeletal muscles but also in many distant organs. The mechanisms responsible for the exercise-induced changes could include oxidative stress or angiotensin II. We previously showed that acute exercise led to apoptosis in kidney but not as a result of oxidative stress. In this study, we examined the role of angiotensin II and its AT1 and AT2 receptors in mediation of exercise-induced apoptosis in kidney. We clearly demonstrated that acute physical exercise induced apoptosis in renal cells of distal convoluted tubuli and cortical and medullary collecting ducts. Moreover, the cells displayed an increased expression of both AT1 and AT2 angiotensin II receptors and of p53 protein. The results suggest that angiotensin II could upregulate p53 expression in renal distal convoluted tubular cells and in the cells collecting ducts via both AT1 and AT2 receptors, which might be the crucial apoptosis-mediating mechanism in kidneys after excessive exercise.

Original languageEnglish
Pages (from-to)459-466
Number of pages8
JournalHistology and Histopathology
Volume21
Issue number4-6
Publication statusPublished - Apr 2006

Keywords

  • Angiotensin II
  • Apoptosis
  • AT1
  • AT2
  • Exercise
  • Kidney

ASJC Scopus subject areas

  • Cell Biology
  • Anatomy
  • Histology
  • Pathology and Forensic Medicine

Fingerprint

Dive into the research topics of 'Exercise-induced apoptosis in rat kidney is mediated by both angiotensin II AT1 and AT2 receptors'. Together they form a unique fingerprint.

Cite this