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Induction of apoptosis during development of hypertensive nephrosclerosis
W Z Ying1, P X Wang, P W Sanders
1Nephrology Research and Training Center, University of Alabama at Birmingham, 35294-0007, USA.
Background:
As the biology of programmed cell death, or apoptosis, is clarified, a role for this process in the pathophysiology of organ dysfunction and fibrosis has been hypothesized. Hypertensive nephrosclerosis represents an important cause of end-stage renal disease. One model of the progressive, noninflammatory, sclerotic renal lesion of hypertension is the Dahl/Rapp salt-sensitive rat, which was examined in this study.
Methods:
Male, Dahl/Rapp salt-sensitive (SS) and Sprague-Dawley rats were placed on either 0.3 or 8.0% NaCl diets for three weeks. Blood pressure was determined, and the kidneys were harvested for histochemical analysis and to obtain total RNA for RNase protection assays and total protein for Western blotting.
Results:
An increase in apoptosis in the glomerular and tubular compartments was observed only in kidneys of SS rats on the high-salt diet. These findings occurred at a time when renal function was markedly impaired and irreversible changes in renal morphology developed. Temporally associated with this increase in apoptosis was augmented expression of pro-apoptotic molecules that included Fas, Bax, and Bcl-XS.
Conclusions:
The inappropriate shift in expression of proteins that facilitate apoptosis in the nephron, along with ongoing cell death that manifested at a time when renal function was deteriorating, supported an important role for this process in development of hypertensive nephrosclerosis.
Insights
High salt intake accelerates kidney damage in salt-sensitive rats by increasing programmed cell death (apoptosis) in the kidneys. This cell death is linked to specific protein changes, contributing to hypertensive nephrosclerosis.
Area of Science:
- Nephrology
- Cell Biology
- Pathophysiology
Background:
- Programmed cell death (apoptosis) is increasingly implicated in organ dysfunction and fibrosis.
- Hypertensive nephrosclerosis is a significant cause of end-stage renal disease.
- The Dahl/Rapp salt-sensitive rat model exhibits progressive sclerotic renal lesions associated with hypertension.
Purpose of the Study:
- To investigate the role of apoptosis in the development of hypertensive nephrosclerosis.
- To examine the effects of a high-salt diet on apoptosis in the Dahl/Rapp salt-sensitive rat model.
Main Methods:
- Male Dahl/Rapp salt-sensitive (SS) and Sprague-Dawley rats were fed either 0.3% or 8.0% NaCl diets for three weeks.
- Blood pressure was measured, and kidneys were analyzed using histochemistry, RNase protection assays, and Western blotting.
Main Results:
- Increased apoptosis was observed in glomerular and tubular compartments of SS rats on a high-salt diet.
- Renal function impairment and irreversible morphological changes coincided with increased apoptosis.
- Expression of pro-apoptotic molecules (Fas, Bax, Bcl-XS) was augmented, correlating with increased apoptosis.
Conclusions:
- The shift in expression of apoptosis-facilitating proteins and ongoing cell death in nephrons contribute to hypertensive nephrosclerosis.
- Apoptosis plays a critical role in the deterioration of renal function observed in this hypertension model.
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