Key result
AT1R blockade alone or co-blockade of AT1R and Mas receptor significantly altered renal blood flow responses to Angiotensin II in 2K1C hypertensive rats following partial renal ischemia/reperfusion.
Why the study?
Renin-angiotensin system activation, partial ischemia/reperfusion injury, and hypertension contribute to acute kidney injury, but the renal vascular responses to Ang II under AT1R or combined AT1R and Mas receptor blockade were unclear.
Population
Thirty-three 2K1C male Wistar rats with systolic blood pressure ≥ 150 mmHg
Comparison
Sham vs IR vs IPC + IR, each receiving losartan vs losartan + A779
Design
Animal experimental study
Authors
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Rat model data on AT1R/Mas blockade in 2K1C IR injury warrant no clinical change; leaves open IPC effects in hypertension.
AT1R and Mas receptors play a significant role in renal blood flow responses to Angiotensin II following partial renal ischemia/reperfusion in 2K1C hypertensive rats.
Karimi et al. (2023) studied 2K1C hypertension with partial ischemia/reperfusion injury (n=33). AT1R blockade (losartan) or co-blockade of AT1R and Mas receptor (A779) vs. Sham was evaluated on Renal blood flow response to Angiotensin II. AT1R blockade alone or co-blockade of AT1R and Mas receptor significantly altered renal blood flow responses to Angiotensin II in 2K1C hypertensive rats following partial renal ischemia/reperfusion.
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