Olmesartan, an Angiotensin II Receptor Blocker, Restores Cerebral Hypoperfusion in Elderly Patients With Hypertension

Nagata, Riya; Kawabe, Kiyokazu; Ikeda, Ken

doi:10.1016/j.jstrokecerebrovasdis.2009.08.004

Cited by 22 publications

(23 citation statements)

References 16 publications

(37 reference statements)

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“…Past work shows blood pressure lowering improves cerebral blood flow and promotes positive neurocognitive outcomes, including decreased risk for dementia. 20,58-61 However, the literature is not consistent as past studies also show limited effects for antihypertensive therapy on the cerebral structure 23 and it is possible that brain damage from long-term periods of uncontrolled hypertension may not be reversible, even with improvements in cerebral blood flow.…”

Section: Discussionmentioning

confidence: 99%

“…Blood pressure lowering in older adults has been suggested to reduce the risk of stroke as well as the development of dementia. 18,19 Antihypertensive treatment is associated with better cerebral perfusion levels 20 and may also reduce risk of brain atrophy and lesions. 21 Nonetheless, the effects of antihypertensive drugs on the brain appear to be complicated.…”

Section: Introductionmentioning

confidence: 99%

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The impact of hypertension on cerebral perfusion and cortical thickness in older adults

Alosco

Gunstad

et al. 2014

Journal of the American Society of Hypertension

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Background Hypertension may increase risk for dementia possibly because of its association with decreased cortical thickness. Disturbed cerebral autoregulation is one plausible mechanism by which hypertension impacts the cerebral structure, but the associations among hypertension, brain perfusion, and cortical thickness are poorly understood. Methods The current sample consisted of 58 older adults with varying levels of vascular disease. Diagnostic history of hypertension and antihypertensive medication status was ascertained through self-report and, when available, confirmed by medical record review. All participants underwent arterial spin labeling and T1-weighted magnetic resonance imaging (MRI) to quantify total and regional cortical perfusion and thickness. Results Analysis of covariance adjusting for medical variables showed that participants with hypertension exhibited reduced temporal and occipital brain perfusion as well as total and regional cortical thickness relative to those without hypertension. The effects of hypertension on total brain perfusion remained unchanged even after adjustment for age, though no such pattern emerged for cortical thickness. Decreased total brain perfusion predicted reduced thickness of the total brain as well as of the frontal, temporal, and parietal lobe cortices. Antihypertensive treatment was not associated with total cerebral perfusion or cortical thickness. Discussion This study provides initial evidence for the adverse effects of a diagnostic history of hypertension on brain hypoperfusion and reduced cortical thickness. Longitudinal studies are needed to investigate the role of hypertension and its interaction with other contributing factors (e.g., age) in the manifestation of cerebral hypoperfusion and reduced cortical thickness.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The impact of hypertension on cerebral perfusion and cortical thickness in older adults

Alosco

Gunstad

et al. 2014

Journal of the American Society of Hypertension

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“…Hypertension has detrimental effects on cerebral blood flow in humans (Lipsitz et al, 2005; Beason-Held et al, 2007; Dai et al, 2008; Efimova et al, 2008; Nagata et al, 2010; Waldstein et al, 2010; Muller et al, 2012). Hypertension is associated with a shift in the autoregulatory curve to the right (Cipolla, 2007; Iadecola and Davisson, 2008).…”

Section: Effects Of Ang II On Cerebrovascular Functionmentioning

confidence: 99%

Effects of angiotensin II on the cerebral circulation: role of oxidative stress

Silva¹,

Faraci²

2013

Front. Physio.

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Oxidative stress has emerged as a key component of many diseases that affect the vasculature. Oxidative stress is characterized as a cellular environment where the generation of oxidant molecules overwhelms endogenous anti-oxidant defense mechanisms. NADPH oxidases are a family of enzymes whose primary purpose is generation of reactive oxygen species (oxidant molecules) and therefore are likely to be key contributors to oxidative stress. Hypertension is associated with oxidative stress in the vasculature and is a major risk factor for stroke and cognitive abnormalities. Angiotensin II (Ang II) is the main effector peptide of the renin-angiotensin system (RAS) and plays a critical role in promoting oxidative stress in the vasculature. In the cerebral circulation, Ang II has been implicated in reactive oxygen species generation, alterations to vasomotor function, impaired neurovascular coupling, inflammation, and vascular remodeling. Furthermore, studies in humans have shown that cerebral blood flow is altered during hypertension and therapeutically targeting the RAS improves cerebral blood flow. Importantly, many of the aforementioned effects have been shown to be dependent on NADPH oxidases. Thus, Ang II, NADPH oxidases and oxidative stress are likely to play key roles in the pathogenesis of hypertension and associated cerebrovascular disease. This review will focus on our current understanding of the contribution of Ang II and NADPH oxidases to oxidative stress in the cerebral circulation.

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“…A study of hypertensive rats by Saavedra et al 20 found that blockade of AT1 receptors increases expression of AT2 receptors, leading to enhanced endothelial nitric oxide synthase activity and nitric oxide production in vascular endothelium. Meanwhile, Nagata et al 21 reported that olmesartan therapy in elderly patients with hypertension improved cerebral hypoperfusion by boosting nitric oxide concentration. Telmisartan, with its high AT1 receptor affinity, likely exhibited this same mechanism to maintain and increase CBF in the present study.…”

Section: Discussionmentioning

confidence: 99%

Effects of telmisartan on the cerebral circulation of hypertensive patients with chronic-stage stroke

et al. 2012

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This prospective study examined the effects of telmisartan, an angiotensin II type I receptor blocker with peroxisome proliferator-activated receptor gamma agonistic action, on blood pressure (BP) control and cerebral circulation in hypertensive patients with chronic-stage stroke. Telmisartan (40 mg per day) was administered to 10 patients with systolic BP (SBP) X140 mm Hg and diastolic BP (DBP) X90 mm Hg at least 4 weeks after lacunar or atherothrombotic infarction. Casual BP and resting cerebral blood flow (CBF) were evaluated at baseline and week 12 using technetium-99 m ethyl cysteinate dimer singlephoton emission computed tomography. Both SBP and DBP declined significantly from 156.4 ± 17.0 to 127.4 ± 6.6 mm Hg and 84.2 ± 14.5 to 74.2 ± 5.2 mm Hg, respectively (Po0.05). Mean CBF (mCBF) in both the left and right cerebral hemispheres did not change, and the mCBF of both the impaired and unimpaired sides of supratentorial lesion patients (n ¼ 6) did not change. Investigation of regional CBF in all patients revealed significant increases in the callosomarginal, precentral, central, parietal, temporal, posterior cerebral, lenticular nucleus, thalamic and hippocampal regions at week 12 (Po0.05). Telmisartan showed good antihypertensive activity in hypertensive patients with chronic-stage stroke without affecting hemispheric blood flow, and it even increased regional CBF in most regions examined.

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Olmesartan, an Angiotensin II Receptor Blocker, Restores Cerebral Hypoperfusion in Elderly Patients With Hypertension

Cited by 22 publications

References 16 publications

The impact of hypertension on cerebral perfusion and cortical thickness in older adults

The impact of hypertension on cerebral perfusion and cortical thickness in older adults

Effects of angiotensin II on the cerebral circulation: role of oxidative stress

Effects of telmisartan on the cerebral circulation of hypertensive patients with chronic-stage stroke

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