Background: Progression of kidney disease is associated with kidney tissue hypoxia. Research on temporal and causal relationships between hypoxia and injury in progression of kidney injury in rodent models has been hampered by lack of methods to measure partial pressure of oxygen (pO2) over extended periods of time in unrestrained animals. Aim of the current study was to examine ability of a newly developed telemetry based technique to record pO2 in rat renal cortex continuously and during modulation by angiotensin II (AngII) and phenylephrine (PE) injections.Methods: Wistar rats (n=8) were instrumented under isoflurane anaesthesia (inhalation, 2-3%) with an oxygen telemeter, i.e. electrodes for continuous pO2 monitoring were implanted in kidney cortex and the telemeter was implanted in the abdomen. In the same procedure a femoral vein catheter was placed for angiotensin II (AngII) and phenylephrine (PE) injections in conscious rats. After 1 week rats were ready for trial. Rats received several doses of AngII and equi-pressor doses of PE with a maximum of 500ng/kg and 1500ng/kg, respectively. To find equi-pressor doses of PE, rats (n=2) were instrumented under isoflurane anaesthesia (inhalation, 2-3%) with a blood pressure telemeter and femoral vein catheter. These rats received the same doses of AngII and PE as the oxygen telemeter instrumented rats.Results: Cortical pO2 values remained stable after recovery from implantation without significant evidence of fibrosis or scarring after 3 weeks of electrode implantation. AngII injections decreased renal cortex tissue pO2 dose-dependently. A dose of 500ng/kg resulted in a decrease of pO2 of 60 ± 15% (P<0.05) and a blood pressure increase of 34 ± 8 mmHg. In contrast equi-pressor doses of PE had no or little effect on cortex tissue pO2. A dose of 1500 ng/kg resulted in a decrease of of pO2 of 14 ± 6% and a blood pressure increase of 39 ± 10 mmHg.Conclusion: This technology appears to be able to track changes in pO2 and provides an opportunity to study the temporal relationships between renal cortical hypoxia and the progression of renal disease. AngII appears to have non-pressor depressing effects on renal oxygenation. Preventing these effects may underlie the renoprotective effect of RAS blockade.