“…The interaction of ACE inhibitors with NSAIDs is a class effect insofar as it concerns reduced angiotensin II activity [7]. It is likely that angiotensin II receptor antagonists, such as losartan, would interact in the same way; animal models of renal artery stenosis support this assumption [10], although no human data are as yet available.…”
“…The interaction of ACE inhibitors with NSAIDs is a class effect insofar as it concerns reduced angiotensin II activity [7]. It is likely that angiotensin II receptor antagonists, such as losartan, would interact in the same way; animal models of renal artery stenosis support this assumption [10], although no human data are as yet available.…”
“…Rats in Groups I, II and III were to be injected subcutaneously with a single 500 ml dose (2.5 mg/kg) of HgCl 2 (99.5% purity; Sigma, St. Louis, MO) in normal (0.9%) saline. Rats in Groups II and IV were to be treated daily by gastric gavage with 30 mg Losartan/kg (Cozaar, Merck & Co., Whitehouse Station, NJ) in normal saline (Abdi & Johns 1997). Rats in Groups III and V were to be treated daily by gavage with 30 mg Enalapril/kg (Renitec, Merck & Co.) in normal saline (Guo et al 2008).…”
Section: Animals and Experimental Designmentioning
confidence: 99%
“…Ang II acts through two receptor subtypes, AT1 and AT2 receptors. Most of the classic physiological effects of Ang II are mediated by the AT1 receptor, including induction of oxidative stress (Abdi & Johns 1997;Garrido & Griendling 2009;Benigni et al 2010). In addition, increased production of Ang II by the effect of Ang I-converting enzyme (ACE) is related to enhanced Ang II-related actions (Abdi & Johns 1997;Benigni et al 2010).…”
Section: Introductionmentioning
confidence: 99%
“…With the advent of drugs such as Losartan that specifically blocks the Ang II AT-1 receptor and Enalapril that blocks ACE activity, it is possible to dissect the physiological roles of the renin-angiotensin system (Abdi & Johns 1997;Donmez et al 2002;Benigni et al 2010;Muñoz et al 2011;Peña et al, 2013). Therefore, the aim of this study was to determine the role of Ang II in the renal oxidative stress and CD8 cell infiltration in rats treated with HgCl 2 using the angiotensin II receptor (AT-1) blocker Losartan and the ACE inhibitor Enalapril.…”
Mercuric chloride (HgCl 2 ) induces kidney damage, in part, through oxidative stress. A role for angiotensin II (Ang II) in pro-inflammatory events in a model of acute HgCl 2 -induced nephropathy was reported. Ang II is a potent oxidative stress inducer; however, its role in oxidative/anti-oxidative events in HgCl 2 -induced nephropathy remains unknown. The aim of this study was to determine the role of Ang II in the oxidative stress and renal infiltration of CD8 + T-cells after an acute HgCl 2 intoxication. Three groups of Sprague Dawley rats were treated with a single subcutaneous dose of 2.5 mg/kg HgCl 2 : for 3 days prior to and for 4 days after that injection, rats in one group received Losartan (30 mg/kg), in another group Enalapril (30 mg/kg) or normal saline in the last group. Two other groups of drug-treated rats received saline in place of HgCl 2 . A final group of rats received saline in place of HgCl 2 and the test drugs. All treatments were via gastric gavage. At 96 h after the vehicle/HgCl 2 injection, blood and kidney samples were harvested. Renal sections were homogenized for measures of malondialdehyde (MDA), reduced glutathione (GSH) and catalase activity. Frozen sections were studied for the presence of superoxide anion (O À 2 ) and CD8 + T-cells. HgCl 2 -treated rats had increased interstitial and tubular expression of O À 2 , high levels of MDA, normal catalase activity and GSH content, increased levels of interstitial CD8 + T-cells and an increased percentage of necrotic tubules. Anti-Ang II treatments diminished the HgCl 2 -induced increases in interstitial O À 2 , CD8 + T-cells and tubular damage and increased catalase and GSH expression above that due to HgCl 2 alone; the HgCl 2 -induced high MDA levels were unaffected by the drugs. These data provide new information regarding the potential role of Ang II in the oxidative stress and renal CD8 + T-cell infiltration that occur during HgCl 2 nephropathy.ARTICLE HISTORY
“…Rats in the Losartan (Cozaar, Merck & Co., Whitehouse Station, NJ) group received this antagonist of AT-1 receptors (angiotensin II receptor type-1) at 30 mg Losartan/kg BW daily by gastric gavage (Abdi and Johns, 1997). Rats in the Enalapril (Renitec, Merck) group received this inhibitor of angiotensin I converting enzyme at 30 mg Losartan/kg BW daily by gavage (Guo et al, 2008).…”
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