Azilsartan medoxomil

Al-Majed, Abdulhakeem A.; Bakheit, Ahmed H.; Al-Muhsin, Ali; Alkahtani, Hamad M.

doi:10.1016/bs.podrm.2019.10.001

Cited by 4 publications

(2 citation statements)

References 30 publications

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“…Azilsartan medoxomi is developed by Takeda and belongs to a new generation of selective AT1 subtype angiotensin II receptor antagonist, and is the prodrug of Azilsartan. A clinical study has reported the stable and durable antihypertensive effects of Azilsartan [ 15 ]. Apart from its antihypertensive effect, other functions claimed for Azilsartan include the prevention of myocardial hypertrophy [ 16 ], vascular remodeling [ 17 ], and renal function damage [ 18 ].…”

Section: Introductionmentioning

confidence: 99%

Azilsartan improves urinary albumin excretion in hypertension mice

Cao,

Zhang,

et al. 2024

Aging

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Hypertension is one of the most important risk factors for chronic kidney diseases, leading to hypertensive nephrosclerosis, including excessive albuminuria. Azilsartan, an angiotensin II type 1 receptor blocker, has been widely used for the treatment of hypertension. However, the effects of Azilsartan on urinary albumin excretion in hypertension haven’t been reported before. In this study, we investigated whether Azilsartan possesses a beneficial property against albuminuria in mice treated with angiotensin II and a high-salt diet (ANG/HS). Compared to the control group, the ANG/HS group had higher blood pressure, oxidative stress, and inflammatory response, all of which were rescued by Azilsartan dose-dependently. Importantly, the ANG/HS-induced increase in urinary albumin excretion and decrease in the expression of occludin were reversed by Azilsartan. Additionally, it was shown that increased fluorescence intensity of FITC-dextran, declined trans-endothelial electrical resistance (TEER) values, and reduction of occludin and krüppel-like factor 2 (KLF2) were observed in ANG/HS-treated human renal glomerular endothelial cells (HrGECs), then prevented by Azilsartan. Moreover, the regulatory effect of Azilsartan on endothelial monolayer permeability in ANG/HS-treated HrGECs was abolished by the knockdown of KLF2, indicating KLF2 is required for the effect of Azilsartan. We concluded that Azilsartan alleviated diabetic nephropathy-induced increase in Uterine artery embolization (UAE) mediated by the KLF2/occludin axis.

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Section: Introductionmentioning

confidence: 99%

Azilsartan improves urinary albumin excretion in hypertension mice

Cao,

Zhang,

et al. 2024

Aging

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“…Lowering blood pressure can reduce the risk of cardiac events, strokes, and kidney problems. Azilsartan, part of the angiotensin receptor blockers (ARBs) family, works by relaxing blood vessels, thus facilitating easier blood flow [ 7 ]. The presence of angiotensin II type 1 receptor (AT1R) blockers in azilsartan elevates angiotensin II (ANG-II) levels, enhancing the activation of angiotensin II type 2 receptor (AT2R).…”

Section: Introductionmentioning

confidence: 99%

Azilsartan improves doxorubicin-induced cardiotoxicity via inhibiting oxidative stress, proinflammatory pathway, and apoptosis

Janabi,

Al-Chlaihawi

2023

JMedLife

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Azilsartan, a known angiotensin receptor blocker, has shown potential in reducing 24-hour blood pressure and may have protective effects against cardiac complications. Increased oxidative stress in cardiac tissue is directly related to the cardiac complications of doxorubicin. This study investigated whether azilsartan could mitigate doxorubicin-induced cardiotoxicity. We divided 28 male rats into four groups: the control group receiving a standard diet and water, the vehicle group given DMSO orally for two weeks, doxorubicin group receiving 2.5 mg/kg of doxorubicin three times a week for two weeks, and azilsartan group treated with 5 mg/kg/day of azilsartan orally and doxorubicin. Doxorubicin-induced cardiotoxicity was evidenced by a significant increase in TNF-α, IL-1β, MDA, and caspase-3 levels and significantly decreased TAC and Bcl-2 levels in the cardiac tissues of treated rats compared to the DMSO and control groups. Azilsartan significantly decreased doxorubicin-induced cardiotoxicity, as evidenced by a decline in serum levels of both TNF-α and IL-1β. Additionally, MDA significantly decreased in the cardiac tissue, although TAC was significantly increased when comparing the azilsartan group to the group receiving doxorubicin-only. These results suggest that azilsartan effectively reduced doxorubicin-induced cardiotoxicity, likely by mitigating apoptosis, inflammation, and oxidative stress in cardiac tissues.

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Blood pressure control, target organ protection and metabolic disorders control using a fixed combination of azilsartan medoxomil + chlorthalidone in hypertensive patients survived after severe and extremely severe COVID-19

et al. 2022

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Objective. Evaluation of the possibility of a fixed combination of azilsartan medoxomil + chlorthalidone in additional angioprotection in patients with arterial hypertension (HTN) and high pulse wave velocity (PWV) after confirmed severe or extremely severe COVID-19 (bilateral polysegmental viral pneumonia) treated by genetically engineered biological drugs, who had not previously received combined antihypertensive therapy.Design and methods. An open observational study lasting 12 weeks included 30 patients, 28–31 days after discharge from the hospital after a severe and extremely severe COVID-19, who received or had not previously received antihypertensive therapy. Patients underwent 24-hour blood pressure (BP) monitoring, applanation tonometry (augmentation index and central BP), measurement of PWV, laboratory tests before and after prescription of a fixed combination of azilsartan medoxomil + chlorthalidone.Results. At baseline, patients showed an increase in office blood pressure to 153,06/92,2 mmHg. After treatment with a fixed combination of azilsartan medoxomil + chlorthalidone, a decrease in systolic BP by 18,47% and diastolic BP by 16,24% was observed. According to ambulatory BP monitoring, the decrease in systolic BP was 19,65% and diastolic BP — 24,68%, PWV decreased by 34,4%, augmentation index — by 9,42%, central systolic BP — by 15,48% (p < 0,05). At baseline, vascular age (VA) was increased to 44,96 years compared to the passport age of 35,03 years. After treatment, there was a significant decrease in VA to 38,74 years (p < 0,01). In addition, the levels of C-reactive protein, fibrinogen, D-dimer, glucose, blood urea nitrogen and uric acid significantly decreased.Conclusions. The fixed combination of azilsartan medoxomil + chlorthalidone provides better control of BP. It also helps to improve vascular elasticity (augmentation index, PWV, central systolic BP, decrease in VA) and to reduce post-infectious inflammation in HTN patients after a severe coronavirus infection.

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Azilsartan medoxomil

Cited by 4 publications

References 30 publications

Azilsartan improves urinary albumin excretion in hypertension mice

Azilsartan improves urinary albumin excretion in hypertension mice

Azilsartan improves doxorubicin-induced cardiotoxicity via inhibiting oxidative stress, proinflammatory pathway, and apoptosis

Blood pressure control, target organ protection and metabolic disorders control using a fixed combination of azilsartan medoxomil + chlorthalidone in hypertensive patients survived after severe and extremely severe COVID-19

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