In vivo imaging of oxidative stress in the kidney of diabetic mice and its normalization by angiotensin II type 1 receptor blocker

Sonta, Toshiyo; Inoguchi, Toyoshi; Matsumoto, Shingo; Yasukawa, Keiji; Inuo, M.; Tsubouchi, Hirohito; Sonoda, Noriyuki; Kobayashi, Kazuo; Utsumi, Hideo; Nawata, Hajime

doi:10.1016/j.bbrc.2005.02.174

Cited by 59 publications

(45 citation statements)

References 33 publications

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“…Oxidative stress in the kidney of diabetic animals estimated by the electron spin resonance imaging technique (Sonta et al, 2005), high-performance liquid chromatography (Nangaku et al, 2003), and an immunohistochemical method (Fan et al, 2004) was ameliorated by ARB treatment.…”

Section: Angiotensin Ii-dependent Hypertensive Models a Angiotensinmentioning

confidence: 99%

The Intrarenal Renin-Angiotensin System: From Physiology to the Pathobiology of Hypertension and Kidney Disease

et al. 2007

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Section: Angiotensin Ii-dependent Hypertensive Models a Angiotensinmentioning

confidence: 99%

The Intrarenal Renin-Angiotensin System: From Physiology to the Pathobiology of Hypertension and Kidney Disease

et al. 2007

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“…To examine this, we applied the technique of in vivo electron spin resonance (ESR) spectroscopy, 22 because the ESR method is a powerful technique for evaluating oxidative stress noninvasively 22,23 and is useful for assessing drug effects when applied in vivo. 24 Using this technique, we examined the effects of chronic oral administration of olmesartan on oxidative stress in the brain of stroke-prone spontaneously hypertensive rats (SHRSP), as well as on blood pressure, heart rate (HR) and urinary norepinephrine (NE) excretion. To examine the direct action of olmesartan on the brain, we also evaluated the effect of intracerebroventricullar administration of RNH-6270 (an active form of olmesartan) on these variables.…”

Section: Introductionmentioning

confidence: 99%

Olmesartan reduces oxidative stress in the brain of stroke-prone spontaneously hypertensive rats assessed by an in vivo ESR method

et al. 2009

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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 À1 day À1 ) or hydralazine (Hyd, 20 mg kg À1 day À1 )/hydrochlorothiazide (HCT, 4.5 mg À1 kg day À1 ) for 30 days (n¼5 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 barrierpermeable spin probe methoxycarbonyl-PROXYL were significantly higher in SHRSP brains than in age-matched normotensive Wistar-Kyoto rat brains (Po0.01; n¼6 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.

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“…The in vivo electron spin resonance (ESR)/spin probe technique is suitable for the examination of free radical reactions in vivo in experimental diseases, as we (Utsumi et al, 1990;Sano et al, 1998;Phumala et al, 1999;Han et al, 2001;Utsumi et al, 2002;Kasazaki et al, 2003a,b;Matsumoto et al, 2003;Yamato et al, 2003;Takeshita et al, 2004;Yasukawa et al, 2004;Sonta et al, 2005) and others (Miura et al, 1997;Kuppusamy et al, 1998;Leonard et al, 2002) have demonstrated. In this technique, the signal decay of the nitroxyl probes mediated by ROS is monitored by ESR spectroscopy.…”

mentioning

confidence: 99%

Noninvasive Mapping of Reactive Oxygen Species by in Vivo Electron Spin Resonance Spectroscopy in Indomethacin-Induced Gastric Ulcers in Rats

Utsumi¹,

Yasukawa²,

Soeda³

et al. 2005

J Pharmacol Exp Ther

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Reactive oxygen species (ROS) are thought to be involved in the gastric ulcer formation induced by indomethacin, a typical nonsteroidal anti-inflammatory drug. However, the location and the time course of ROS generation remain unknown. To assess the sites of ROS generation, we applied the noninvasive measurement of ROS to indomethacin-treated rats. By giving orally a membrane-permeable or impermeable probe, the spectra were collected as a function of time by in vivo 300-MHz electron spin resonance (ESR) spectroscopy. The ESR signal-decay rates of membrane-permeable probes, hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl (TEMPO) and 3-methoxycarbonyl-2,2,5,5-tetramethyl-pyrrolidine-1-oxyl, in the gastric mucosal region were significantly enhanced 1 h after indomethacin treatment, and they both caused the protection of ulcer formation; however, membrane-impermeable probes, carboxy-and trimethylammonium-TEMPO, which did not exhibit the enhanced signal decay, had no effect on ulcer formation. The enhanced signal decay in the gastric mucosa was suppressed by coadministration of the antioxidants tiron or dimethylthiourea with the nitroxyl probe. The results suggest that the enhanced signal-decay rates in the gastric ulcers observed by in vivo ESR are associated with protective effects. The enhanced signal decay caused by ROS generation in stomach, contributing to the ulcer formation induced by indomethacin, is also suggested to occur at the gastric mucus layer or the interface or the intracellular compartment of epithelial cells. Overall, these results show the potentials of noninvasive assessment of ROS production and the sites of damage by in vivo ESR using nitroxyl probes directed to specific subcellular regions.Nonsteroidal anti-inflammatory drugs (NSAIDs) have defervescence, analgesia, and anti-inflammatory effects, and their clinical applications to rheumatism, osteoporosis, and osteoarthritis have been increasing. Indomethacin ([1-(4-chlorobenzoyl)-5-methoxy-2-methyl-1H-indol-3-yl] acetic acid) is one of the most widely used NSAIDs in the world because the anti-inflammatory effect of indomethacin on carrageenin-induced edema is approximately 30 times higher than that of aspirin (2-acetoxybenzoic acid) (Winter et al., 1963). NSAIDs cause therapeutic effects by the suppression of prostaglandin biosynthesis via the inhibition of cyclooxygenase (COX) gene expression. This class of agents is also known to cause significant gastrointestinal damage (Vane, 1971). It is known that the COX enzymes have isozymes of three types (Chandrasekharan et al., 2002), and the inhibition of COX-1 in gastric mucosa has been thought to be related with the gastric ulcer formation induced by NSAIDs (Wallace et al., 1998), because COX-1 is involved in maintaining the integrity of gastric mucosa, the increment of

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In vivo imaging of oxidative stress in the kidney of diabetic mice and its normalization by angiotensin II type 1 receptor blocker

Cited by 59 publications

References 33 publications

The Intrarenal Renin-Angiotensin System: From Physiology to the Pathobiology of Hypertension and Kidney Disease

The Intrarenal Renin-Angiotensin System: From Physiology to the Pathobiology of Hypertension and Kidney Disease

Olmesartan reduces oxidative stress in the brain of stroke-prone spontaneously hypertensive rats assessed by an in vivo ESR method

Noninvasive Mapping of Reactive Oxygen Species by in Vivo Electron Spin Resonance Spectroscopy in Indomethacin-Induced Gastric Ulcers in Rats

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