Hydroxyl Radical Mediates the Augmented Angiotensin II Responses in Thoracic Aorta of Spontaneously Hypertensive Rats

Deshmukh, Aaishwarya B.; Patel, Natvarlal J.; Patel, Rohit B.

doi:10.1159/000100867

Cited by 5 publications

(4 citation statements)

References 67 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…On the other hand, in animal models, hypertension also induced hyperreactivity to Ang II. In spontaneously hypertensive rats, hydroxyl radical stress induced hyperreactivity to Ang II (23).…”

Section: Discussionmentioning

confidence: 94%

Nitric Oxide Modulates Reactivity to Angiotensin II in Internal Mammary Arterial Grafts in Hytertensive Patients Without Associated Risk Factors

Turoni

Marañón

Proto³

et al. 2011

Clinical and Experimental Hypertension

View full text Add to dashboard Cite

We investigated the effects of extraendothelial nitric oxide (NO) on angiotensin II (Ang II) reactivity in internal mammary artery (IMA) rings, as well as the impact of hypertension without associated risk factors in this response. Vascular reactivity, NO levels, and resting membrane potentials were determined in hypertensive (HT) and normotensive (NT) IMA rings. Only rings with endothelial dysfunction were included. Ang II produced a dose-dependent contraction that was higher in HT rings. Response to Ang II was potentiated by Nω-nitro L-arginine methyl ester (L-NAME) in NT but not in HT rings. The antioxidant agents tempol and diphenyleneiodonium (DPI) reverted the hyperreactivity to Ang II in HT rings. Extraendothelial NO was present in both NT and HT rings. However, NT rings showed higher values. L-NAME and S-methyl-L-thiocitrulline inhibited NO release in all cases. L-arginine reverted this inhibition. Both tempol and DPI increased NO release in both NT and HT rings. The number of vascular smooth muscle cells (VSMC) and anti-α-actin positive areas were lower in HT than in NT rings, without variations in wall thickness or wall/lumen ratio. With regard to resting membrane potential, we found in HT rings that the depolarization induced by Ang II was abolished by tempol. These findings suggest that extraendothelial NO counterregulates Ang II contractility in IMA rings; however, its action could be altered in hypertensive situations even though the patients did not have associated risk factors. We suggest two mechanisms: increased oxidative stress and a decreased ability of nNOS in VSMC to produce NO.

show abstract

Section: Discussionmentioning

confidence: 94%

Nitric Oxide Modulates Reactivity to Angiotensin II in Internal Mammary Arterial Grafts in Hytertensive Patients Without Associated Risk Factors

Turoni

Marañón

Proto³

et al. 2011

Clinical and Experimental Hypertension

View full text Add to dashboard Cite

show abstract

“…Hydroxyl radical stress augments angiotensin II-induced contractile responses in the thoracic aorta of spontaneously hypertensive rats. Edaravone could serve as an adjuvant antioxidant therapy for the vascular complications of hypertension by attenuating these enhanced vascular responses [96]. Hypertension induces cardiac hypertrophy and ROS also act as second messengers to develop cardiac hypertrophy in hypertensive model mice [97].…”

Section: Oxidative Stress and Edaravone Efficacy In Cardiovascularmentioning

confidence: 99%

The Efficacy of Edaravone (Radicut), a Free Radical Scavenger, for Cardiovascular Disease

Kikuchi

Tancharoen

Takeshige

et al. 2013

IJMS

103

View full text Add to dashboard Cite

Edaravone was originally developed as a potent free radical scavenger, and has been widely used to treat acute ischemic stroke in Japan since 2001. Free radicals play an important role in the pathogenesis of a variety of diseases, such as cardiovascular diseases and stroke. Therefore, free radicals may be targets for therapeutic intervention in these diseases. Edaravone shows protective effects on ischemic insults and inflammation in the heart, vessel, and brain in experimental studies. As well as scavenging free radicals, edaravone has anti-apoptotic, anti-necrotic, and anti-cytokine effects in cardiovascular diseases and stroke. Edaravone has preventive effects on myocardial injury following ischemia and reperfusion in patients with acute myocardial infarction. Edaravone may represent a new therapeutic intervention for endothelial dysfunction in the setting of atherosclerosis, heart failure, diabetes, or hypertension, because these diseases result from oxidative stress and/or cytokine-induced apoptosis. This review evaluates the potential of edaravone for treatment of cardiovascular disease, and covers clinical and experimental studies conducted between 1984 and 2013. We propose that edaravone, which scavenges free radicals, may offer a novel option for treatment of cardiovascular diseases. However, additional clinical studies are necessary to verify the efficacy of edaravone.

show abstract

“…Edaravone injection, in the current study, attenuated that increase in blood pressure and the cardiac structure. Many studies have addressed the effectiveness of edaravone as a cardio-protectant, especially in ischemia/reperfusion injury [ 33 , 45 , 55 ], possibly via its hydroxyl radicals quenching properties [ 12 ] and its anti-inflammatory effect [ 26 ]. The maternal blood urea and creatinine levels were significantly increased in this study, this was accompanied by renal histopathological alterations in the RUPP mothers.…”

Section: Discussionmentioning

confidence: 99%

Effect of edaravone on pregnant mice and their developing fetuses subjected to placental ischemia

Atallah

Yamashita

Abe

2021

Reprod Biol Endocrinol

View full text Add to dashboard Cite

Growing evidence indicates that reduced uterine perfusion pressure (RUPP) triggers the cascade of events leading to preeclampsia. Edaravone is a powerful free radical scavenger used for the treatment of ischemia/reperfusion diseases due to its anti-oxidative stress and anti-inflammatory properties. Here we investigate the effect of edaravone (3 mg/kg) on different maternal and fetal outcomes of RUPP-induced placental ischemia mice model. RUPP surgery was performed on gestation day (GD) 13 followed by edaravone injection from GD14 to GD18, sacrifice day. The results showed that edaravone injection significantly decreased the maternal blood pressure (113.2 ± 2.3 mmHg) compared with RUPP group (131.5 ± 1.9 mmHg). Edaravone increased fetal survival rate (75.4%) compared with RUPP group (54.4%), increased fetal length, weights, and feto-placental ratio (7.2 and 5.7 for RUPP and RUPP-Edaravone groups, respectively) compared with RUPP group. In addition, RUPP resulted in many fetal morphological abnormalities as well as severe delayed ossification, however edaravone decreased the morphological abnormalities and increased the ossification of the fetal endoskeleton. Edaravone improved the histopathological structure of the maternal kidney and heart as well as decreased the elevated blood urea and creatinine levels (31.5 ± 0.15 mg/dl (RUPP), 25.6 ± 0.1 mg/dl (RUPP+edaravone) for urea and 5.4 ± 0.1 mg/dl (RUPP), 3.5 ± 0.1 mg/dl (RUPP+edaravone) for creatinine) and decreased cleaved caspase-3 expression in the maternal kidney. In conclusion, this study demonstrated that our RUPP mice model recapitulated preeclampsia symptoms and edaravone injection ameliorated most of these abnormalities suggesting its effectiveness and potential application in preeclampsia treatment regimes.

show abstract

Hydroxyl Radical Mediates the Augmented Angiotensin II Responses in Thoracic Aorta of Spontaneously Hypertensive Rats

Cited by 5 publications

References 67 publications

Nitric Oxide Modulates Reactivity to Angiotensin II in Internal Mammary Arterial Grafts in Hytertensive Patients Without Associated Risk Factors

Nitric Oxide Modulates Reactivity to Angiotensin II in Internal Mammary Arterial Grafts in Hytertensive Patients Without Associated Risk Factors

The Efficacy of Edaravone (Radicut), a Free Radical Scavenger, for Cardiovascular Disease

Effect of edaravone on pregnant mice and their developing fetuses subjected to placental ischemia

Contact Info

Product

Resources

About