Premium
Mitochondrial ROS in the Brain Contributes to Angiotensin II‐induced Hypertension
Author(s) -
Jun Joo Yun,
Zubcevic Jasenka,
Shi Peng,
Qi Yanfei,
Sumners Colin,
Raizada Mohan
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.854.2
Increased oxidative stress in CNS circumventricular organs is implicated in angiotensin II (AngII) induced hypertension. Here, our objective was to test the hypothesis that mitochondrial ROS in CV relevant brain regions is critical to the establishment of neurogenic hypertension in this animal model. The mitochondrial‐targeted antioxidant mitoTEMPO was used to scavenge ROS especially produced from mitochondria. Intracerebroventricular (ICV) infusion of mitoTEMPO (150ug/kg/day) for 4 weeks significantly reduced blood pressure in SD rats made hypertensive by s.c. infusion of Ang II (200ng/kg/min) [control: 98±2 mmHg (n=5), AngII: 177±6 mmHg (n=4), AngII+mitoTEMPO: 146±12 mmHg (n=5)]. In addition, spectral analysis showed increases in sympathetic vasomotor activity in the AngII treated group at week 3 and week 4, an effect that was blocked by ICV infusion of mitoTEMPO (ΔLF (SBP) control: −0.23024 ms 2 /mmHg 2 , AngII: 0.9756 ms 2 /mmHg 2 , mitoTEMPO: −0.12711 ms 2 /mmHg 2 ). Furthermore, spontaneous baroreceptor reflex gain was reduced in AngII infused rats (ΔsBRG (PI): −0.1964 ms/mmHg) but not in the mitoTEMPO ICV treated rats (ΔsBRG (PI): −0.0726 ms/mmHg) compared to controls (ΔsBRG(PI): +0.1837 ms/mmHg). These data suggest that mitochondrial ROS in CV relevant brain regions are at least in part responsible for the establishment of neurogenic hypertension.