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Exogenous and endogenous angiotensin-II decrease renal cortical oxygen tension in conscious rats by limiting renal
Tonja W Emans1,2, Ben J Janssen3, Maximilian I Pinkham4
1Nephrology and Hypertension, University Medical Centre Utrecht, Utrecht, The Netherlands.
The Journal of Physiology
|July 19, 2016
Summary
Angiotensin-II (AngII) reduces renal cortical oxygen levels, contributing to kidney disease progression. This effect, mediated by AT1 receptors, highlights AngII
Area of Science:
- Nephrology and Renal Physiology
- Cardiovascular Research
- Hypoxia and Ischemia Studies
Background:
- The role of hypoxia in kidney disease initiation and progression is not fully understood.
- Existing methods for measuring renal tissue oxygen tension are limited.
- Angiotensin-II (AngII) is implicated in kidney disease, but its direct effect on renal oxygenation requires clarification.
Purpose of the Study:
- To develop and validate a wireless method for continuous measurement of renal cortical tissue oxygen tension (PO2) in unrestrained rats.
- To investigate the effects of exogenous and endogenous AngII on renal cortical PO2.
- To determine the contribution of AngII-induced renal hypoxia to the development of kidney disease.
Main Methods:
- Development of a wireless telemetry system with a carbon paste electrode for chronic PO2 measurement in rat renal cortex.
- Administration of exogenous AngII and phenylephrine to conscious rats to assess their impact on renal cortical PO2.
- Utilisation of Cyp1a1Ren2 transgenic rats to activate the endogenous renin-angiotensin system and evaluate the effects of AT1 receptor blockade.
Main Results:
- The developed method provided stable, continuous PO2 measurements for over two weeks and reliably detected acute changes in cortical oxygenation.
- Intravenous AngII dose-dependently reduced renal cortical PO2, with a significantly greater effect than equi-pressor doses of phenylephrine.
- Activation of the endogenous renin-angiotensin system in transgenic rats reduced cortical PO2, an effect rapidly reversible by AT1 receptor antagonism.
Conclusions:
- Angiotensin-II significantly reduces renal cortical oxygen tension, primarily by decreasing renal oxygen delivery.
- AngII-induced renal hypoxia, mediated via AT1 receptors, precedes structural pathology in a transgenic rat model.
- The findings suggest that AngII-promoted renal hypoxia may play a crucial role in the initiation and progression of chronic kidney disease.
