Key Points
- To determine whether chronic systemic elevations of angiotensin II regulate AT1 receptor mRNA and protein expression in a tissue-specific pattern during sustained hypertension.
- Sprague-Dawley rats were continuously infused subcutaneously with either vehicle or angiotensin II at 80 ng/min for 13 days using osmotic minipumps.
- AT1A mRNA and protein abundance in renal, hepatic, and adrenal tissues were quantified on day 12 using semiquantitative RT-PCR with GAPDH controls, Southern blot hybridization, and Western blotting.
- Angiotensin II infusion raised systolic blood pressure to 186±12 mm Hg versus 121±2 mm Hg in vehicle controls and suppressed plasma renin activity to 0.1±0.01 versus 4.9±0.9 ng Ang I/mL/h (P<0.05).
- Adrenal AT1A/GAPDH mRNA ratios increased to 0.49±0.04 in angiotensin II-infused rats compared with 0.36±0.02 in controls (P<0.05), whereas kidney (0.19±0.05 vs 0.26±0.03) and liver (2.8±0.9 vs 3.0±0.5) ratios remained similar.
- Western blot analysis demonstrated that AT1 protein levels in renal and hepatic tissues were unchanged between angiotensin II-infused and vehicle-treated animals.
Structured PICO
PPopulationSprague-Dawley rats
IInterventionAngiotensin II (80 ng/min) infused subcutaneously via osmotic minipump for 13 days
CComparatorVehicle infused subcutaneously via osmotic minipump for 13 days
OOutcomeAT1A/GAPDH mRNA ratios and AT1 protein levels in kidney, liver, and adrenal glandssurrogate
In a rat model of Ang II-induced hypertension, renal and liver AT1 receptor expression is maintained rather than downregulated, which may contribute to progressive increases in arterial pressure.