PMID- 19763130
OWN - NLM
STAT- MEDLINE
DCOM- 20100224
LR  - 20171116
IS  - 1348-4214 (Electronic)
IS  - 0916-9636 (Linking)
VI  - 32
IP  - 12
DP  - 2009 Dec
TI  - Olmesartan reduces oxidative stress in the brain of stroke-prone spontaneously 
      hypertensive rats assessed by an in vivo ESR method.
PG  - 1091-6
LID - 10.1038/hr.2009.160 [doi]
AB  - We previously showed that oxidative stress in the brain is involved in the neural 
      mechanisms of hypertension. Therefore, olmesartan, an angiotensin type 1 receptor 
      blocker, might affect oxidative stress in the brains of stroke-prone 
      spontaneously hypertensive rats (SHRSP). Here, we evaluated the effects of 
      olmesartan treatment using an in vivo electron spin resonance (ESR)/spin probe 
      technique. Two groups of SHRSP were treated with either olmesartan (10 mg kg(-1) 
      day(-1)) or hydralazine (Hyd, 20 mg kg(-1) day(-1))/hydrochlorothiazide (HCT, 4.5 
      mg (-1)kg day(-1)) for 30 days (n=5 for each). Systolic blood pressure decreased 
      similarly in both groups after treatment. Heart rate and urinary norepinephrine 
      (NE) excretion increased in rats treated with Hyd/HCT, but not in those treated 
      with olmesartan. The in vivo ESR signal decay rates of the blood-brain 
      barrier-permeable spin probe methoxycarbonyl-PROXYL were significantly higher in 
      SHRSP brains than in age-matched normotensive Wistar-Kyoto rat brains (P<0.01; 
      n=6 for each). Olmesartan attenuated the ESR signal decay rates in SHRSP brains, 
      but Hyd/HCT did not. Intracerebroventricular infusion of active form of 
      olmesartan, RNH-6270, reduced blood pressure and NE excretion, and the ESR signal 
      decay rate was reduced in SHRSP brains. These findings indicate that olmesartan 
      has anti-oxidative property in the brain without stimulating reflex-mediated 
      sympathetic activity in SHRSP.
FAU - Araki, Shuichiro
AU  - Araki S
AD  - Department of Cardiovascular Medicine, Kyushu University, Maidashi, Higashi-ku, 
      Fukuoka, Japan.
FAU - Hirooka, Yoshitaka
AU  - Hirooka Y
FAU - Kishi, Takuya
AU  - Kishi T
FAU - Yasukawa, Keiji
AU  - Yasukawa K
FAU - Utsumi, Hideo
AU  - Utsumi H
FAU - Sunagawa, Kenji
AU  - Sunagawa K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090918
PL  - England
TA  - Hypertens Res
JT  - Hypertension research : official journal of the Japanese Society of Hypertension
JID - 9307690
RN  - 0 (Angiotensin II Type 1 Receptor Blockers)
RN  - 0 (Antihypertensive Agents)
RN  - 0 (Imidazoles)
RN  - 0 (Tetrazoles)
RN  - 0J48LPH2TH (Hydrochlorothiazide)
RN  - 26NAK24LS8 (Hydralazine)
RN  - 8W1IQP3U10 (olmesartan)
RN  - EC 1.6.3.- (NADPH Oxidases)
RN  - X4W3ENH1CV (Norepinephrine)
SB  - IM
CIN - Hypertens Res. 2009 Dec;32(12):1047-8. PMID: 19893566
MH  - Angiotensin II Type 1 Receptor Blockers/*pharmacology
MH  - Animals
MH  - Antihypertensive Agents/pharmacology
MH  - Blood Pressure/drug effects
MH  - Brain/*blood supply/metabolism
MH  - Electron Spin Resonance Spectroscopy/methods
MH  - Heart Rate/drug effects
MH  - Hydralazine/pharmacology
MH  - Hydrochlorothiazide/pharmacology
MH  - Hypertension/*drug therapy/metabolism
MH  - Imidazoles/*pharmacology
MH  - Male
MH  - NADPH Oxidases/metabolism
MH  - Norepinephrine/urine
MH  - Oxidative Stress/*drug effects
MH  - Rats
MH  - Rats, Inbred SHR
MH  - Rats, Inbred WKY
MH  - Stroke/*metabolism/prevention & control
MH  - Tetrazoles/*pharmacology
EDAT- 2009/09/19 06:00
MHDA- 2010/02/25 06:00
CRDT- 2009/09/19 06:00
PHST- 2009/09/19 06:00 [entrez]
PHST- 2009/09/19 06:00 [pubmed]
PHST- 2010/02/25 06:00 [medline]
AID - hr2009160 [pii]
AID - 10.1038/hr.2009.160 [doi]
PST - ppublish
SO  - Hypertens Res. 2009 Dec;32(12):1091-6. doi: 10.1038/hr.2009.160. Epub 2009 Sep 
      18.