Publication: Exercise-induced apoptosis in rat kidney is mediated by both angiotensin II AT1 and AT2 receptors
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Date
2006
Authors
Podhorska-Okolow, M. ; Dziegiel, Piotr ; Gomulkiewicz, A. ; Kisiela, D. ; Dolinska-Krajewska, B. ; Jethon, Z. ; Carraro, U. ; Zabel, M.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
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.
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