The role of reactive oxygen species in the modulation of the contraction induced by angiotensin II in carotid artery from diabetic rat

Pernomian, Laena; Gomes, Mayara Santos; Restini, Carolina Baraldi Araújo; Ramalho, Leandra Náira Zambelli; Tirapelli, Carlos Renato; Oliveira, Ana Maria de

doi:10.1016/j.ejphar.2011.12.036

Cited by 25 publications

(36 citation statements)

References 40 publications

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“…Restenosis could persistently damage the cerebral irrigation by carotid pathways during type I-diabetes since carotid flow is drastically reduced by the enhanced local resistance resultant from diabetic endothelial and muscular dysfunction [9,11,12]. Nevertheless, our previous findings show that this circulatory complication is counterregulated by balloon neurocompensation, which prevents further damages in carotid cerebral irrigation by restoring contralateral carotid flow.…”

Section: Introductionmentioning

confidence: 89%

“…The fasting glucose levels were determined from rat tail blood samples prior to (day 0) or 48 h (day 2) after STZ injection by using a one-touch glucometer (LifeScan Inc., Milpitas, CA, USA). Rats were considered diabetic when presented a glycemia higher than 300 mg/dL (Table 1) [9,11,12]. Twenty-eight days after STZ-injection [22] balloon injury was performed in the left (ipsilateral) carotid artery of anesthetized rats [4,[7][8][9].…”

Section: Experimental Designmentioning

confidence: 99%

“…Likewise, to investigate if the H 2 O 2 levels were generated from the dismutation of superoxide anion (O 2 − ) (eventually generated by Nox), carotid arteries were also pretreated with tiron (O 2 − scavenger, 0.1 mmol/L) [8,9,11,12] for 30 min before sample homogenization.…”

Section: Alk5 Phospho-smad2/3 Nox4 and Mas Receptor Expressionmentioning

confidence: 99%

“…Isolated common carotid arteries were longitudinally sectioned and endothelial cells were mechanically isolated by gentle friction with a plastic stem in plates containing Hanks' solution (composition in mmol/L: CaCl 2 1.6; MgSO 4 1.0; NaCl 145.0; KCl 5.0; NaH 2 PO 4 0.5; dextrose 10.0; HEPES 10.0, pH 7.4). The cell suspensions were centrifuged at 1.375 ×g for 5 min [8,9,11,12,25] and the supernatant was stored at − 20°C until use. Each n comprised a pool of fifteen carotid arteries.…”

Section: Tgfβ 1 Quantitative Measurementmentioning

confidence: 99%

See 3 more Smart Citations

Vasoprotective effects of neurocompensatory response to balloon injury during diabetes involve the improvement of Mas signaling by TGFβ1 activation

Gomes

Pernomian

Moreira

et al. 2015

Vascular Pharmacology

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Section: Introductionmentioning

confidence: 89%

Section: Experimental Designmentioning

confidence: 99%

Section: Alk5 Phospho-smad2/3 Nox4 and Mas Receptor Expressionmentioning

confidence: 99%

Section: Tgfβ 1 Quantitative Measurementmentioning

confidence: 99%

See 2 more Smart Citations

Vasoprotective effects of neurocompensatory response to balloon injury during diabetes involve the improvement of Mas signaling by TGFβ1 activation

Gomes

Pernomian

Moreira

et al. 2015

Vascular Pharmacology

Self Cite

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“…The main effect of Ang II is vasoconstriction by [32][33][34] increasing sympathetic tone [35] and arginine vasopressin (AVP) release [36][37][38] through stimulation of AT1 receptors mainly present in the vasculature. Activation of Ang II receptors and even nonreceptor pathways has been presented in a review by Touyz and Berry [39].…”

Section: Ang II and Its Main Signaling Pathways To Produce Cardio Andmentioning

confidence: 99%

Free Radicals and Biomarkers Related to the Diagnosis of Cardiorenal Syndrome

Restini¹,

Pereira²,

Geleilete³

2016

Free Radicals and Diseases

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The National Heart, Lung, and Blood Institute Working Group has postulated the cardiorenal syndrome (CRS) as an interaction between the kidneys and the cardiovascular system in which therapy to relieve congestive heart failure (HF) symptoms is limited by the further worsening renal function. CRS is classified from type I to V, taking into account the progression of the symptoms in terms of mechanisms, clinical conditions, and biomarkers. Experimental and clinical studies have shown the kidney as both a trigger and a target to sympathetic nervous system (SNS) overactivity. Renal damage and ischemia, activation of the renin angiotensin aldosterone system (RAAS), and dysfunction of nitric oxide (NO) system are associated with kidney adrenergic activation. Indeed, the imbalances of RAAS and/or SNS share an important common process in CRS: the activation and production of free radicals, especially reactive oxygen species (ROS). The present chapter addresses connections of the free radicals as potential biomarkers as the imbalances in the RAAS and the SNS are developed. Understanding the involvement of free radicals in CRS may bring knowledge to design studies in order to develop accurate pharmacological interventions.

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Rho-kinase and the nitric oxide pathway modulate basilar arterial reactivity to acetylcholine and angiotensin II in streptozotocin-induced diabetic mice

Islam

Dao

Miyamoto

et al. 2017

Naunyn-Schmiedeberg's Arch Pharmacol

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Diabetes mellitus comprises a heterogeneous group of metabolic disorders with underlying hyperglycemia and secondary cardiovascular complications. Growing evidence suggests that vascular dysfunction is among the most important causes of diabetic cardiovascular disease. Therefore, we determined whether streptozotocin (STZ)-induced diabetes in mice affects blood pressure and cerebral arterial responsiveness to angiotensin (Ang) II and acetylcholine (ACh), which are important modulators of cerebrovascular autoregulation. Diabetes was induced using a single intraperitoneal injection of STZ (50 mg/kg). Blood pressure was measured in conscious mice using the indirect tail-cuff method. Functional studies of the isolated arteries' response to vasoactive substances were performed using a micro-organ-bath system at 60 days after STZ injection. Systolic, diastolic, and mean blood pressures significantly increased at days 45 and 60 in the STZ-induced diabetic mice. In the isolated basilar arteries, ACh-induced relaxation, which is dependent on nitric oxide (NO) production from endothelial cells, decreased. In contrast, Ang II-induced contraction, mediated via rho-kinase activation in the smooth muscle, increased in the diabetic mice. There was significantly greater relaxation in the precontracted isolated basilar arteries of diabetic mice that had been treated with Y27632, a rho-kinase inhibitor, than in the control mice arteries. Pretreatment with Nω-nitro-L-arginine (L-NAME), an NO synthase inhibitor, significantly enhanced Ang II-induced contraction and Y27632-induced relaxation in the control basilar arteries but not in the STZ-induced diabetic mice arteries. These results suggest that decreased NO bioavailability and enhanced rho-kinase activity in basilar arteries contribute to altered reactivity to ACh and Ang II, respectively, in STZ-induced diabetic mice.

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The role of reactive oxygen species in the modulation of the contraction induced by angiotensin II in carotid artery from diabetic rat

Cited by 25 publications

References 40 publications

Vasoprotective effects of neurocompensatory response to balloon injury during diabetes involve the improvement of Mas signaling by TGFβ1 activation

Vasoprotective effects of neurocompensatory response to balloon injury during diabetes involve the improvement of Mas signaling by TGFβ1 activation

Free Radicals and Biomarkers Related to the Diagnosis of Cardiorenal Syndrome

Rho-kinase and the nitric oxide pathway modulate basilar arterial reactivity to acetylcholine and angiotensin II in streptozotocin-induced diabetic mice

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