Inhibition of cardiovascular cell proliferation by angiotensin receptor blockers: are all molecules the same?

Benson, Stephen C.; Iguchi, Rumiko; Ho, Christopher; Yamamoto, Kōichi; Kurtz, Theodore W.

doi:10.1097/hjh.0b013e3282f56ba5

Cited by 34 publications

(27 citation statements)

References 18 publications

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“…These include direct measurement of binding to and activation of PPAR-g (Fujimoto et al, 2004;Schupp et al, 2004) and inhibition of ARB responses by PPAR-g antagonists such as GW9662 (Willson et al, 2000), AT1R knock-out mice (Rong et al, 2010), and PPAR-g knockdown by siRNA approaches (Nakaya et al, 2007;Scalera et al, 2008;Walcher et al, 2008). More indirect evidence for a role of PPAR-g in ARB effects comes from comparisons of ARBs with and without alleged PPAR-g agonism (Benson et al, 2008;Scalera et al, 2008) and comparison of ARB effects with those of established PPAR-g agonists such as pioglitazone or rosiglitazone (Zanchi et al, 2007;Walcher et al, 2008).…”

Section: A Peroxisome Proliferator-activated Receptorsmentioning

confidence: 99%

A Systematic Comparison of the Properties of Clinically Used Angiotensin II Type 1 Receptor Antagonists

et al. 2013

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Section: A Peroxisome Proliferator-activated Receptorsmentioning

confidence: 99%

A Systematic Comparison of the Properties of Clinically Used Angiotensin II Type 1 Receptor Antagonists

et al. 2013

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“…Telmisartan has also been reported to inhibit the proliferation of CV cells. 9 Both telmisartan and losartan have platelet antiaggregatory activity that is not shared by valsartan's, candesartan's, or losartan's major metabolite, EXP3174. [10][11][12][13] Losartan also reduces uric acid, an end-product of purine metabolism linked to the progression of renal disease 14 and increased CV risk 15 and implicated in the development of hypertension in children.…”

Section: Pharmacologic Actions Unique To Specific Arbsmentioning

confidence: 99%

Angiotensin Receptor Blockers: Pharmacology, Efficacy, and Safety

Taylor

Siragy

Nesbitt

2011

The Journal of Clinical Hypertension

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Key Points and Practical Recommendations• The angiotensin receptor blockers are highly effective antihypertensive agents that are also particularly well tolerated.• There are no major differences in efficacy or other clinical characteristics among older drugs in this class, although some of the newer agents may more effectively reduce blood pressure than older agents.• Major randomized clinical trials have demonstrated that angiotensin receptor blockers provide significant outcomes benefits in conditions such as diabetic nephropathy, chronic heart failure or heart failure following myocardial infarction, hypertension with left ventricular hypertrophy and in patients whose histories of previous events or complicated diabetes puts them at high cardiovascular risk.• In treating hypertension, angiotensin receptor blockers can be used as first-line therapy or added at later stages of treatment titration.• These drugs are very effective in combination with thiazide diuretics or calcium channel blockers and there are several single-pill, fixed-dose combinations of angiotensin receptor blockers with hydrochlorothiazide, amlodipine, or aliskiren. These combinations can be given as initial therapy (where appropriate) or later in the course of treatment. Three-drug combinations (angiotensin receptor blocker plus amlodipine plus hydrochlorothiazide and angiotensin receptor blocker plus aliskiren plus hydrochlorothiazide) are also available. J Clin Hypertens (Greenwich). 2011;13:677-686. Ó2011 Wiley Periodicals, Inc.The renin-angiotensin-aldosterone system (RAAS) plays an important role in protecting vertebrates against cardiovascular collapse due to hypotension and volume loss in the event of traumatic injury that involves blood loss. In certain humans, however, inappropriate or exaggerated activity of the RAAS contributes to the development of hypertension and the initiation of a molecular cascade in tissues with consequent injury to critical organs such as the brain, kidneys, heart, and blood vessels. 1-3 As understanding of the pathologic role of the RAAS in hypertensive vascular disease has unfolded during the past century, so has the interest in developing drugs that could interdict specific components of the RAAS. The first of the RAAS-blocking drugs to become commercially available were the aldosterone antagonists in the 1970s, followed by the angiotensin-converting enzyme (ACE) inhibitors in the 1980s and the angiotensin II receptor blockers (ARBs) in the 1990s. Unlike ACE inhibitors that inhibit the conversion of angiotensin I to II, ARBs bind to the angiotensin II AT 1 receptor, thereby inhibiting the cellular actions of angiotension II mediated by the receptor in which the tissue is located. During the past 20 years, studies in the laboratory and clinic have documented that ARBs, either alone or in combination with drugs of other classes, reduce blood pressure (BP) in hypertensive animals and humans; reduce rates of myocardial infarction (MI), stroke, and progression of renal impairment; and positively impact oth...

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“…Angiotensin II binds to the angiotensin receptors AT 1 and AT 2 . Activation of AT 1 receptors is associated with endothelial dysfunction (13) , vasoconstriction (13) , cell proliferation (14) , platelet aggregation (15) , inhibition of nitric oxide synthase (16) , aldosterone release (17) , cognitive and behavioural processes such as depression, anxiety, enhanced learning and memory (18)(19)(20) , dementia (20) and increases in reactive oxygen species (21) .…”

mentioning

confidence: 99%

Effects of green tea, black tea and Rooibos tea on angiotensin-converting enzyme and nitric oxide in healthy volunteers

Persson

Hägg

et al. 2010

Public Health Nutr.

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Objective: Tea has been reported to reduce cardiovascular mortality, but the underlying mechanisms are largely unknown. The aim of the current project was to investigate the effect of green tea (Japanese Sencha), black tea (Indian Assam B.O.P.) and Rooibos tea (South Africa) on angiotensin-converting enzyme (ACE) and nitric oxide (NO). Design: Seventeen healthy volunteers received a single oral dose of 400 ml green tea, black tea or Rooibos tea in a randomized, three-phase, crossover study. ACE activity and NO concentration were measured (at 0, 30, 60 and 180 min) in all phases. ACE activity was analysed by means of a commercial radioenzymatic assay. Nitrite was analysed as a marker of NO concentration. In addition, ACE genotype was determined using a PCR method. Results: Oral intake of a single dose of Rooibos tea significantly inhibited ACE activity after 30 min (P , 0?01) and after 60 min (P , 0?05). A significant inhibition of ACE activity was seen with green tea for the ACE II genotype 30 min after intake of the tea (P , 0?05) and for the ACE ID genotype 60 min after intake (P , 0?05). A significant inhibition of ACE activity was also seen with Rooibos tea for the ACE II genotype 60 min after intake (P , 0?05). No significant effect on NO concentration was seen. Conclusions: These results suggest that green tea and Rooibos tea may have cardiovascular effects through inhibition of ACE activity.

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Inhibition of cardiovascular cell proliferation by angiotensin receptor blockers: are all molecules the same?

Cited by 34 publications

References 18 publications

A Systematic Comparison of the Properties of Clinically Used Angiotensin II Type 1 Receptor Antagonists

A Systematic Comparison of the Properties of Clinically Used Angiotensin II Type 1 Receptor Antagonists

Angiotensin Receptor Blockers: Pharmacology, Efficacy, and Safety

Effects of green tea, black tea and Rooibos tea on angiotensin-converting enzyme and nitric oxide in healthy volunteers

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