Effect of the angiotensin II receptor blocker olmesartan on the development of murine acute myocarditis caused by coxsackievirus B3

2006 ◽  
Vol 110 (3) ◽  
pp. 379-386 ◽  
Author(s):  
Yoshinori Seko
Keyword(s):  
Angiotensin Ii ◽  
Fas Ligand ◽  
Acute Myocarditis ◽  
Coxsackievirus B3 ◽  
Myocardial Inflammation ◽  
Myocardial Tissue ◽  
Angiotensin Ii Receptor Blocker ◽  
Protective Effects ◽  
Ang Ii ◽  
Angiotensin Ii Receptor

Ang II (Angiotensin II) has been shown to play a pivotal role in the pathophysiology of various organs, especially the cardiovascular system. The effects of ARBs (Ang II receptor blockers) in the treatment of hypertension, congestive heart failure and myocardial fibrosis have been analysed extensively in human trials, as well as animal models, and the focus of interest is now directed to its pleiotropic effects, especially on inflammatory disorders. To investigate the effects of a new ARB, olmesartan, on immune-mediated myocardial injury, the protective effects of olmesartan on the development of murine acute myocarditis caused by CVB3 (coxsackievirus B3) were analysed. Olmesartan and a non-specific vasodilator hydralazine lowered systolic blood pressure of mice on day 7 after virus inoculation to a similar extent. Olmesartan significantly decreased myocardial inflammation compared with controls, whereas hydralazine significantly increased this. Olmesartan significantly decreased the expression of IFN-γ (interferon-γ), FasL (Fas ligand), iNOS (inducible nitric oxide synthase) and PFP (pore-forming protein) in myocardial tissue, indicating that olmesartan suppressed the activation of infiltrating killer lymphocytes. Olmesartan also decreased the expression of CVB3 genomes in myocardial tissue as well as serum levels of 8-OHdG (8-hydroxy-2′-deoxyguanosine), a biomarker of oxidative-stress-induced DNA damage. The findings suggest that olmesartan prevents myocardial damage and may improve the prognosis of patients with acute myocarditis; however, further investigations are needed before clinical use.

scholarly journals Protective Effects of an Angiotensin II Receptor Blocker and a Long-Acting Calcium Channel Blocker against Cardiovascular Organ Injuries in Hypertensive Patients

2005 ◽  
Vol 28 (4) ◽  
pp. 351-359 ◽  
Author(s):  
Toshihiko ISHIMITSU ◽  
Tsutomu KOBAYASHI ◽  
Takeaki HONDA ◽  
Masaki TAKAHASHI ◽  
Junichi MINAMI ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Channel Blocker ◽  
Receptor Blocker ◽  
Angiotensin Ii Receptor Blocker ◽  
Protective Effects ◽  
Angiotensin Ii Receptor ◽  
Hypertensive Patients ◽  
Long Acting

scholarly journals Molecular targeting therapy with angiotensin II receptor blocker for prostatic cancer

2011 ◽  
pp. 3-13
Author(s):  
Hiroji Uemura ◽  
Hitoshi Ishiguro ◽  
Yoshinobu Kubota
Keyword(s):  
Prostate Cancer ◽  
Angiotensin Ii ◽  
Cancer Cells ◽  
Stromal Cells ◽  
Angiotensin Ii Receptor Blocker ◽  
Ang Ii ◽  
Angiotensin Ii Receptor ◽  
Targeting Therapy ◽  
Receptor Blockers ◽  
Prostatic Diseases

Angiotensin II (Ang-II) plays a key role as a vasoconstrictor in controlling blood pressure and electrolyte/fluid homeostasis. Recently it has also been shown that this peptide is a cytokine, acting as a growth factor in cardiovascular and stromal cells. In addition, the physiological function of Ang-II seems to be similar in prostate cancer and stromal cells. It is widely assumed that Ang-II facilitates the growth of both cells, and its receptor blockers (ARBs) have the potential to inhibit the growth of various cancer cells and tumors through the Ang-II receptor type 1 (AT1 receptor). The mechanism of cell growth inhibition by ARBs has been considered to be that of suppression of the signal transduction systems activated by growth factors or cytokines in prostate cancer cells, and suppression of angiogenesis. This review highlights the possible use of ARBs as novel agents for prostatic diseases including prostate cancer and benign hypertrophy, and covers related literature.

scholarly journals Long-term, up to 18 months, protective effects of the angiotensin II receptor blocker telmisartan on Epirubin-induced inflammation and oxidative stress assessed by serial strain rate

SpringerPlus ◽  
2013 ◽  
Vol 2 (1) ◽  
pp. 198 ◽  
Author(s):  
Mariele Dessì ◽  
Clelia Madeddu ◽  
Alessandra Piras ◽  
Christian Cadeddu ◽  
Giorgia Antoni ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Angiotensin Ii ◽  
Strain Rate ◽  
Receptor Blocker ◽  
Angiotensin Ii Receptor Blocker ◽  
Protective Effects ◽  
Angiotensin Ii Receptor ◽  
And Oxidative Stress

scholarly journals Potential role of ACE2 in coronavirus disease 2019 (COVID-19) prevention and management

2020 ◽  
Vol 8 (1) ◽  
pp. 9-19 ◽  
Author(s):  
Mengyuan Liu ◽  
Ting Wang ◽  
Yun Zhou ◽  
Yutong Zhao ◽  
Yan Zhang ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Potential Role ◽  
Human Monoclonal Antibody ◽  
Harmful Effect ◽  
Spike Protein ◽  
Angiotensin Ii Receptor Blocker ◽  
Ang Ii ◽  
Angiotensin Ii Receptor ◽  
Novel Coronavirus

AbstractCOVID-19 is the current public health threat all over the world. Unfortunately, there is no specific prevention and treatment strategy for this disease. We aim to explore the potential role of angiotensin-converting enzyme 2 (ACE2) in this regard through this literature review. As a crucial enzyme of renin-angiotensin-aldosterone system (RAAS), ACE2 not only mediates the virus entry but also affects the pathophysiological process of virus-induced acute lung injury (ALI), as well as other organs’ damage. As interaction of COVID-19 virus spike and ACE2 is essential for virus infection, COVID-19-specific vaccine based on spike protein, small molecule compound interrupting their interaction, human monoclonal antibody based on receptor-binding domain, and recombinant human ACE2 protein (rhuACE2) have aroused the interests of researchers. Meanwhile, ACE2 could catalyze angiotensin II (Ang II) to form angiotensin 1-7 (Ang 1-7), thus alleviates the harmful effect of Ang II and amplifies the protection effect of Ang1-7. ACE inhibitor and angiotensin II receptor blocker (ARB) have been shown to increase the level of expression of ACE2 and could be potential strategies in protecting lungs, heart, and kidneys. ACE2 plays a very important role in the pathogenesis and pathophysiology of COVID-19 infection. Strategies targeting ACE2 and its ligand, COVID-19 virus spike protein, may provide novel method in the prevention and management of novel coronavirus pneumonia.

Protective Effects of the Angiotensin II Receptor Blocker Losartan on Cisplatin-Induced Kidney Injury

Chemotherapy ◽  
2009 ◽  
Vol 55 (6) ◽  
pp. 399-406 ◽  
Author(s):  
Samira Saleh ◽  
Afaf A. Ain-Shoka ◽  
Ebtehal El-Demerdash ◽  
Marwa M. Khalef
Keyword(s):  
Angiotensin Ii ◽  
Kidney Injury ◽  
Receptor Blocker ◽  
Angiotensin Ii Receptor Blocker ◽  
Protective Effects ◽  
Angiotensin Ii Receptor

scholarly journals Seasonal dosage-dependent hypersensitivity to the angiotensin II receptor blocker, losartan. A case report and review

2013 ◽  
Author(s):  
Donald R Forsdyke
Keyword(s):  
Angiotensin Ii ◽  
Dosage Adjustment ◽  
Early Years ◽  
Receptor Subtype ◽  
Angiotensin Ii Receptor Blocker ◽  
Close Monitoring ◽  
Ang Ii ◽  
Angiotensin Ii Receptor ◽  
Geographical Regions ◽  
Long Term Treatment

Since it has been in clinical use for two decades, individual data permitting evaluation of the long-term treatment of hypertension with losartan, which blocks the dominant angiotensin-II receptor (AT 1 R), should now be available. In the present case, by dosage adjustment according to daily home blood pressure (BP) readings, a mild degree of hypertension discovered during routine examination was kept in the 130/80 (mm Hg) range over an 11 year period (2003-2013). In the early years, control was achieved with 12.5 – 25.0 mg/day and dosage adjustment was seldom needed on a seasonal basis. However, on increasing to 50 mg/day, a profound downward adjustment to 0 – 12.5 mg/day was required in hot weather. The adjustment may have prevented recurrence of drug-induced postural hypotension and renal colic. Whether the adjustment facilitated an increased nocturnal BP, as suggested by some ambulatory BP studies, was not examined. A working hypothesis, consistent with animal experiments, is that under conditions of heat-stress (e.g. vascular dilation, salt loss), there is increased expression of a countervailing, losartan-insensitive, receptor subtype (AT 2 R). By lowering BP in response to angiotensin-II, AT 2 R would facilitate fine-tuningof the AT 1 R-mediated vasoconstriction that supports BP when superficial veins dilate to enhance body cooling. This AT 2 R activity might be sufficient to explain a small summertime BP dip found in normal human subjects whose Ang II levels are not increased. The dip would be greatly enhanced when Ang II levels were increased at higher losartan dosages. Close monitoring of losartan dosage may be necessary for those living in, or travelling to, geographical regions where temperatures are seasonally or continually high, and for those engaging in activities that involve such exposure (e.g. hot yoga, Turkish baths).

Protective effects of the angiotensin II receptor blocker telmisartan on epirubicin-induced inflammation, oxidative stress, and early ventricular impairment

2010 ◽  
Vol 160 (3) ◽  
pp. 487.e1-487.e7 ◽  
Author(s):  
Christian Cadeddu ◽  
Alessandra Piras ◽  
Giovanni Mantovani ◽  
Martino Deidda ◽  
Mariele Dessì ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Angiotensin Ii ◽  
Receptor Blocker ◽  
Angiotensin Ii Receptor Blocker ◽  
Protective Effects ◽  
Angiotensin Ii Receptor

scholarly journals Renin Inhibitor Aliskiren Improves Impaired Nitric Oxide Bioavailability and Protects Against Atherosclerotic Changes

Hypertension ◽  
2008 ◽  
Vol 52 (3) ◽  
pp. 563-572 ◽  
Author(s):  
Toshio Imanishi ◽  
Hiroto Tsujioka ◽  
Hideyuki Ikejima ◽  
Akio Kuroi ◽  
Shigeho Takarada ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Renin Inhibitor ◽  
Receptor Blocker ◽  
Angiotensin Ii Receptor Blocker ◽  
Protective Effects ◽  
Angiotensin Ii Receptor ◽  
Plaque Area ◽  
Direct Renin Inhibitor ◽  
Valsartan Group ◽  
Atherosclerotic Changes

We investigated whether aliskiren, a direct renin inhibitor, improves NO bioavailability and protects against spontaneous atherosclerotic changes. We also examined the effects of cotreatment with aliskiren and valsartan, an angiotensin II receptor blocker, on the above-mentioned outcomes. Watanabe heritable hyperlipidemic rabbits were treated with vehicle (control), aliskiren, valsartan, or aliskiren plus valsartan for 8 weeks. Then, acetylcholine-induced NO production was measured as a surrogate index of endothelium protective function, and both superoxide and vascular peroxynitrite were measured. Tetrahydrobiopterin in aortic segments was assessed by high-performance liquid chromatography with fluorescence detection. Plaque area was quantified by histology. Increase in plasma NO concentration in response to intra-aortic acetylcholine infusion was significantly greater in all of the test groups than in controls. Aliskiren+valsartan cotreatment increased acetylcholine-induced NO by 6.2 nmol/L, which was significantly higher than that with either aliskiren or valsartan alone. Vascular superoxide and peroxynitrite levels were both significantly higher in controls and significantly lower in the aliskiren+valsartan group than in the aliskiren or valsartan group. The highest tetrahydrobiopterin levels were observed after aliskiren+valsartan cotreatment. Histology of the thoracic aorta revealed that the plaque area was significantly decreased with combination therapy compared with monotherapy. Treatment with a direct renin inhibitor has protective effects on endothelial function and atherosclerotic changes. Furthermore, cotreatment with a direct renin inhibitor and an angiotensin II receptor blocker has additive protective effects on both.

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