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angiotensin/acidente vascular cerebral
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Use of Angiotensin-Converting Enzyme Inhibitors and Angiotensin Receptor Blockers for Geriatric Ischemic Stroke Patients: Are the Rates Right?
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BACKGROUND
Our objective is to estimate the effects associated with higher rates of renin-angiotensin system antagonists, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers (ACEI/ARBs), in secondary prevention for geriatric (aged >65 years) patients with new ischemic strokes
Angiotensin-converting enzyme insertion/deletion polymorphism and the risk of ischemic stroke in a South Indian population.
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Stroke is one of the most complex diseases with several subtypes, arising from numerous gene-gene and gene-environmental interactions. The aim of our study was to investigate whether the insertion/deletion polymorphism in Angiotensin-converting enzyme gene is associated with ischemic stroke in a
Angiotensin II type 1 receptor antagonist and angiotensin-converting enzyme inhibitor altered the activation of Cu/Zn-containing superoxide dismutase in the heart of stroke-prone spontaneously hypertensive rats.
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Although angiotensin II type 1 (AT1) receptor antagonists and angiotensin-converting enzyme (ACE) inhibitors are known to reduce both reactive oxygen species (ROS) generated by activated NAD(P)H oxidase and vascular remodeling in hypertension, the effects of AT1 receptor antagonists or ACE
Aldosterone breakthrough during angiotensin II receptor antagonist therapy in stroke-prone spontaneously hypertensive rats.
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Aldosterone breakthrough during ACE inhibitor therapy has been reported. This study investigates changes in plasma aldosterone concentration (PAC) and its mechanism and effects on target organ damage during long-term angiotensin II type 1 (AT1) receptor antagonist (AT1A) therapy in hypertensive
Angiotensin II type 2 receptor stimulation initiated after stroke causes neuroprotection in conscious rats.
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We have demonstrated previously that pretreatment with an angiotensin II type 2 receptor (AT(2)R) agonist is neuroprotective against a subsequent stroke independent of any changes in blood pressure. Therefore, in the current study, we have examined the potential neuroprotective effect of AT(2)R
Potential of the angiotensin receptor blockers (ARBs) telmisartan, irbesartan, and candesartan for inhibiting the HMGB1/RAGE axis in prevention and acute treatment of stroke.
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Stroke is a major cause of mortality and disability worldwide. The main cause of stroke is atherosclerosis, and the most common risk factor for atherosclerosis is hypertension. Therefore, antihypertensive treatments are recommended for the prevention of stroke. Three angiotensin receptor blockers
Angiotensin II type 2 receptor stimulation with compound 21 improves neurological function after stroke in female rats: a pilot study.
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The angiotensin II type 2 receptor (AT2R) agonist, compound 21 (C21), has been shown to be neurovascularly protective after ischemic stroke in male rats. In the current study, we aim to study the impact of C21 treatment on female rats. Young female Wistar rats were subjected to different
Post-stroke angiotensin II type 2 receptor activation provides long-term neuroprotection in aged rats.
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Activation of the angiotensin II type 2 receptor (AT2R) by administration of Compound 21 (C21), a selective AT2R agonist, induces neuroprotection in models of ischemic stroke in young adult animals. The mechanisms of this neuroprotective action are varied, and may include direct and indirect effects
Expression of angiotensin II AT2 receptor in the acute phase of stroke in rats.
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A male Wistar rat model of stroke (middle cerebral artery occlusion; MCAO) was used to study the angiotensin II (Ang II) receptor subtype 2 (AT2) gene expression by reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemical staining. After permanent occlusion of the middle
Influence of on-going treatment with angiotensin-converting enzyme inhibitor or angiotensin receptor blocker on the outcome of patients treated with intravenous rt-PA for ischemic stroke.
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BACKGROUND
Many patients who receive intravenous (i.v.) recombinant tissue-plasminogen activator (rt-PA) for acute cerebral ischemia were under angiotensin-converting enzyme inhibitors (ACE-Is) or angiotensin receptor blockers (ARBs) at stroke onset. ACE-Is and ARBs have neuroprotective properties
Direct stimulation of angiotensin II type 2 receptor initiated after stroke ameliorates ischemic brain damage.
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BACKGROUND
Stroke is a leading cause of death and disability; however, meta-analysis of randomized controlled trials of blood pressure-lowering drugs in acute stroke has shown no definite evidence of a beneficial effect on functional outcome. Accumulating evidence suggests that angiotensin II type 1
Centrally administered angiotensin-(1-7) increases the survival of stroke-prone spontaneously hypertensive rats.
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UNASSIGNED
What is the central question of this study? Activation of angiotensin-converting enzyme 2, resulting in production of angiotensin-(1-7) and stimulation of its receptor, Mas, exerts beneficial actions in a number cardiovascular diseases, including ischaemic stroke. A potential beneficial
Effect of prestroke use of angiotensin-converting enzyme inhibitors alone versus combination with antiplatelets and statin on ischemic stroke outcome.
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BACKGROUND
Angiotensin-converting enzyme inhibitors (ACEIs), antiplatelets (APs), and statin are increasingly being prescribed for ischemic stroke prevention.
OBJECTIVE
The objective of the study was to examine whether previous combination therapy of ACEI with AP and/or statin has additive effect
Impact of the additive effect of angiotensin-converting enzyme inhibitors and /or statins with antiplatelet medication on mortality after acute ischaemic stroke.
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There has been recent interest in combining antiplatelets, angiotensin-converting enzyme inhibitors (ACEIs) and statins in primary and secondary ischaemic stroke prevention. This observational study was performed to evaluate the impact of adding ACEIs and/or statins to antiplatelets on post-stroke
Possible pathophysiologic mechanisms supporting the superior stroke protection of angiotensin receptor blockers compared to angiotensin-converting enzyme inhibitors: clinical and experimental evidence.
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Stroke is a major cause of death and disability and its incidence increases linearly with age and the level of systolic and diastolic blood pressure. Stroke, besides being a cause of long-term disability for the affected person, also imposes a significant burden on society and healthcare costs.
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