Renin-angiotensin system

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Characterization of the cardiac renin angiotensin system in oophorectomized and estrogen-replete mRen2.Lewis rats.

Characterization of the cardiac renin angiotensin system in oophorectomized and estrogen-replete mRen2.Lewis rats.

The cardioprotective effects of estrogen are well recognized, but the mechanisms remain poorly understood. Accumulating evidence suggests that the local cardiac renin-angiotensin system (RAS) is involved in the development and progression of cardiac hypertrophy, remodeling, and heart failure. Estrogen attenuates the effects of an activated circulating RAS; however, its role in regulating the cardiac RAS is unclear. Bilateral oophorectomy (OVX; n = 17) or sham-operation (Sham; n = 13) was performed in 4-week-old, female mRen2.Lewis rats. At 11 weeks of age, the rats were randomized and received either 17 b- estradiol (E2, 36 m g/pellet, 60-day release, n = 8) or vehicle (OVX-V, n = 9) for 4 weeks. The rats were sacrificed, and blood and hearts were used to determine protein and/or gene expression of circulating and tissue RAS components. E2 treatment minimized the rise in circulating angiotensin (Ang) II and aldosterone produced by loss of ovarian estrogens. Chronic E2 also attenuated OVX-associated increases in cardiac Ang II, Ang-(1–7) content, chymase gene expression, and mast cell number. Neither OVX nor OVX+E2 altered cardiac expression or activity of renin, angiotensinogen, angiotensin-converting enzyme (ACE), and Ang II type 1 receptor (AT1R). E2 treatment in OVX rats significantly decreased gene expression of MMP-9, ACE2, and Ang-(1–7) mas receptor, in comparison to sham-operated and OVX littermates. E2 treatment appears to inhibit upsurges in cardiac Ang II expression in the OVX-mRen2 rat, possibly by reducing chymase-dependent Ang II formation. Further studies are warranted to determine whether an E2-mediated reduction in cardiac chymase directly contributes to this response in OVX rats.
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Palmitoylethanolamide treatment reduces blood pressure in spontaneously hypertensive rats: involvement of cytochrome p450-derived eicosanoids and renin angiotensin system.

Palmitoylethanolamide treatment reduces blood pressure in spontaneously hypertensive rats: involvement of cytochrome p450-derived eicosanoids and renin angiotensin system.

Palmitoylethanolamide (PEA), a peroxisome proliferator-activated receptor-α agonist, has been demonstrated to reduce blood pressure and kidney damage secondary to hyperten- sion in spontaneously hypertensive rat (SHR). Currently, no information is available con- cerning the putative effect of PEA on modulating vascular tone. Here, we investigate the mechanisms underpinning PEA blood pressure lowering effect, exploring the contribution of epoxyeicosatrienoic acids, CYP-dependent arachidonic acid metabolites, as endothelium- derived hyperpolarizing factors (EDHF), and renin angiotensin system (RAS) modulation. To achieve this aim SHR and Wistar-Kyoto rats were treated with PEA (30 mg/kg/day) for five weeks. Functional evaluations on mesenteric bed were performed to analyze EDHF- mediated vasodilation. Moreover, mesenteric bed and carotid were harvested to measure CYP2C23 and CYP2J2, the key isoenzymes in the formation of epoxyeicosatrienoic acids, and the soluble epoxide hydrolase, which is responsible for their degradation in the corre- sponding diols. Effect of PEA on RAS modulation was investigated by analyzing angioten- sin converting enzyme and angiotensin receptor 1 expression. Here, we showed that EDHF-mediated dilation in response to acetylcholine was increased in mesenteric beds of PEA-treated SHR. Western blot analysis revealed that the increase in CYP2C23 and CYP2J2 observed in SHR was significantly attenuated in mesenteric beds of PEA-treated SHR, but unchanged in the carotids. Interestingly, in both vascular tissues, PEA significant- ly decreased the soluble epoxide hydrolase protein level, accompanied by a reduced serum concentration of its metabolite 14-15 dihydroxyeicosatrienoic acid, implying a reduction in epoxyeicosatrienoic acid hydrolisis. Moreover, PEA treatment down-regulated angiotensin receptor 1 and angiotensin converting enzyme expression, indicating a reduction in angio- tensin II-mediated effects. Consistently, a damping of the activation of angiotensin receptor
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The renin-angiotensin system is modulated by swimming training depending on the age of spontaneously hypertensive rats

The renin-angiotensin system is modulated by swimming training depending on the age of spontaneously hypertensive rats

Total RNA was isolated from LV tissue with a Trizol reagent (GIBCO Invitrogen). Total RNA concentration and integrity were assessed and the real-time polymerase chain reaction was performed. The mRNA expression of the renin-angiotensin system components were assessed by oligonucleotide primers as follows: for rAgtF: 5′- TCTACCCTTTTGGGTGCTG-3′, rAgtR: 5′-CAAGGAGGATGCTGTTGAGA-3′, expected product size: 88 bp. The expression of Ppia (peptidylprolyl isomerase A – cyclophilin A) (rPpiaF: 5´-AATGCTGGACCAAACACAAA-3´, rPpiaR: 5´-CCTTCTTTCACCTTCCCAAA-3´, expected product size: 101 bp) was measured as an internal control for a sample variation in RT reaction. Real-Time PCR amplifications were performed with an ABI Prism 7700 Sequence Detection System (Applied Biosystems) by using SYBR Green PCR Master Mix (Applied Biosystems). The results were quantified as Ct values, where Ct is defined as the threshold cycle of the polymerase chain reaction at which the amplified product is first detected. Values for the control gene (Ppia) were used to standardize the results in order to compensate for differences in RNA content among the samples. To compare the level of gene expression in the trained group to the level in the control group, the following formula was applied e=2 −ΔΔCt .
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Effects of Exercise Training on Circulating and Skeletal Muscle Renin-Angiotensin System in Chronic Heart Failure Rats

Effects of Exercise Training on Circulating and Skeletal Muscle Renin-Angiotensin System in Chronic Heart Failure Rats

reduced AngII uptake in the soleus muscle [44], because AT1 expression was substantially lower in the exercise-trained rats. In plantaris muscle, exercise training also reduced AngII concentra- tion, but caused no changes in AT1 expression. These findings raise the question that the mechanisms underlying the reduction in AngII in plantaris muscle and soleus muscle are different. Someone could suggest that the reduction in AngII in the plantar muscle is due to the decrease in AngI cleavage. In fact, we found that AngI concentration in plantar muscle was significantly lower in exercise-trained CHF compared to that in untrained CHF rats. Our data clearly demonstrate that there is a mismatch between circulating and skeletal muscle RAS. Elevation in AngII concen- tration was found in the skeletal muscle, but not in the circulation. These findings are consistent with those of previous studies that show that local RAS becomes activated in tissues in CHF [5–8]. The increase in the plasma AngII concentration seems to occur Figure 3. Circulating renin angiotensin system (RAS) in sedentary and exercise-trained Sham and CHF rats. CHF, chronic heart failure; -S, Sedentary; -Ex, Exercise-trained. A, Angiotensin II; B, Angiotensin-(1–7); C, Ang-(1–7)/AngII ratio; D, ACE activity; E, ACE2 activity. *P,0.05 vs. Sham- S; {P,0.05 vs. CHF-S.
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Renin-angiotensin system blockers regulate the metabolism of isolated fat cells in vitro

Renin-angiotensin system blockers regulate the metabolism of isolated fat cells in vitro

There are two main pathways through which glycerol can be synthesized: from glucose during glycolysis; and from glucose metabolites (mainly lactate and pyruvate) through glyceroneogenesis. In the first case, glucose is diverted from the initial phase of glycolysis, when dihydroxyacetone phosphate is converted into glycerol- 3-phosphate by glycerol-3-phosphate dehydrogenase. In glyceroneogenesis, the pyruvate generated from glycoly- sis is then redirected back to dihydroxyacetone phosphate through the action of phosphoenol pyruvate carboxy- kinase (PEPCK) (20). Although PEPCK is mostly recog- nized as a liver gluconeogenic enzyme, its concentration Figure 4. Glycerol glucose incorporation of isolated fat cells previously treated with renin-angiotensin system blockers (A) aliskiren, (B) captopril and (C) losartan. Cells were incubated with increasing concentrations of insulin for 60 min at 37°C. D-[U- 14 C]-glucose
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Local fetal lung renin angiotensin system as a target to treat congenital diaphragmatic hernia

Local fetal lung renin angiotensin system as a target to treat congenital diaphragmatic hernia

Antenatal stimulation of lung growth is a reasonable approach to treat congenital diaphragmatic hernia (CDH), a disease characterized by pulmonary hypoplasia and hypertension. Several evidences from the literature demonstrated a possible in- volvement of renin-angiotensin system (RAS) during fetal lung development. Thus, the expression pattern of renin, angiotensin-con- verting enzyme, angiotensinogen, type 1 (AT 1 ) and type 2 (AT 2 ) receptors of angiotensin II (ANGII) was assessed by immunohisto- chemistry throughout gestation, whereas the function of RAS in the fetal lung was evaluated using fetal rat lung explants. These were morphometrically analyzed and intracellular pathway alterations assessed by Western blot. In nitrofen-induced CDH model, pregnant rats were treated with saline or PD-123319. In pups, lung growth, protein/DNA ratio, radial saccular count, epithelial dif- ferentiation and lung maturation, vascular morphometry, right ventricular hypertrophy and overload molecular markers, gasom- etry and survival time were evaluated. Results demonstrated that all RAS components were constitutively expressed in the lung during gestation and that ANGII had a stimulatory effect on lung branching, mediated by AT 1 receptor, through p44/42 and Akt phosphorylation. This stimulatory effect on lung growth was mimicked by AT 2 -antagonist (PD-123319) treatment. In vivo antenatal PD-123319 treatment increased lung growth, ameliorated indirect parameters of pulmonary hypertension, improved lung function and survival time in nonventilated CDH pups, without maternal or fetal deleterious effects. Therefore, this study demonstrated a local and physiologically active RAS during lung morphogenesis. Moreover, selective inhibition of AT 2 receptor is presented as a putative antenatal therapy for CDH.
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Role of renin-angiotensin system in development of heart failure induced by myocardial infarction in rats

Role of renin-angiotensin system in development of heart failure induced by myocardial infarction in rats

Myocardial infarction (MI) often evokes left ventricu- lar dilatation associated with hypertrophy and fibroses of non-infarcted myocardium. Compensatory mecha- nisms, that help the compromised tissue in the early steps of the ischemic insult, are detrimental in the chronic stage of this disease (Francis 1985). Because one of these compensatory mechanisms, the circulating and lo- cal renin-angiotensin system, has long been considered

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Regression of cardiac hypertrophy in the SHR by combined renin-angiotensin system blockade and dietary sodium restriction

Regression of cardiac hypertrophy in the SHR by combined renin-angiotensin system blockade and dietary sodium restriction

Altered operation of the renin-angiotensin-aldosterone system (RAAS) and dietary sodium intake have been identified as independent risk factors for cardiac hypertrophy. The way in which sodium intake and the operation of the renin-angiotensin-aldosterone system interact in the pathogenesis of cardiac hypertrophy is poorly understood. The aims of this study were to investigate the cardiac effects of the renin-angiotensin system (RAS) blockade in the spontaneously hypertensive rat (SHR), using co-treatment with an angiotensin II receptor blocker (ARB) and an angiotensin-converting enzyme (ACE) inhibitor with different sodium intakes. Our experiments with SHR show that, at high levels of sodium intake (4.0%), aggressive RAS blockade treatment with candesartan (3 mg/kg) and perindopril (6 mg/kg) does not result in regression of cardiac hypertrophy. In contrast, RAS blockade coupled with reduced sodium diet (0.2%) significantly regresses cardiac hypertrophy, impairs animal growth and is associated with elevated plasma renin and dramatically suppressed plasma
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H(2)S inhibits hyperglycemia-induced intrarenal renin-angiotensin system activation via attenuation of reactive oxygen species generation.

H(2)S inhibits hyperglycemia-induced intrarenal renin-angiotensin system activation via attenuation of reactive oxygen species generation.

The abnormality in intrarenal renin-angiotensin system (RAS) plays a crucial role in the onset and development of DN. The over activation in intrarenal RAS has been reported to be associated with glomerular enlargement and secondary glomerulosclerosis, tubular epithelial to mesenchymal transition, interstitial fibroblast proliferation and extracellular matrix (ECM) deposition [18,19]. Currently, the inhibitors of RAS, including angiotensin converting enzyme inhibitor (ACEI) or angiotensin II (AngII) type I receptor (AT1) blockers (ARB), have been used as first line medication in the clinical treatment of DN. Data suggest that there is an interaction between ROS overproduction and RAS activation [β0-ββ]. However, the exact mechanism has not been fully elucidated. Recently, Lu M et al reported that NaHS treatment inhibits elevation in renin activity and blunted blood pressure increase in β-kidney 1-clip hypertensive rats [βγ]. This experiment is aimed at investigating the effects of H β S production suppression under
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Long-term effects of early overnutrition in the heart of male adult rats: role of the renin-angiotensin system.

Long-term effects of early overnutrition in the heart of male adult rats: role of the renin-angiotensin system.

To analyze the long-term effects of early overfeeding on the heart and coronary circulation, the effect of ischemia- reperfusion (I/R) and the role of the renin-angiotensin system (RAS) was studied in isolated hearts from control and overfed rats during lactation. On the day of birth litters were adjusted to twelve pups per mother (controls) or to three pups per mother (overfed). At 5 months of age, the rats from reduced litters showed higher body weight and body fat than the controls. The hearts from these rats were perfused in a Langendorff system and subjected to 30 min of ischemia followed by 15 min of reperfusion (I/R). The myocardial contractility (dP/dt) and the coronary vasoconstriction to angiotensin II were lower, and the expression of the apoptotic marker was higher, in the hearts from overfed rats compared to controls. I/R reduced the myocardial contractily, the coronary vasoconstriction to angiotensin II and the vasodilatation to bradykinin, and increased the expression of (pro)renin receptor and of apoptotic and antiapoptotic markers, in both experimental groups. I/ R also increased the expression of angiotensinogen in control but not in overfed rats. In summary, the results of this study suggest that early overnutrition induces reduced activity of the RAS and impairment of myocardial and coronary function in adult life, due to increased apoptosis. Ischemia-reperfusion produced myocardial and coronary impairment and apoptosis, which may be related to activation of RAS in control but not in overfed rats, and there may be protective mechanisms in both experimental groups.
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EL SISTEMA RENINA−ANGIOTENSINA DESDE LA CIRCULACIÓN HASTA LA CÉLULA: IMPLICACIONES MÁS ALLÁ DE LA HIPERTENSIÓN / The renin−angiotensin system from circulation to the cell: implications beyond hypertension

EL SISTEMA RENINA−ANGIOTENSINA DESDE LA CIRCULACIÓN HASTA LA CÉLULA: IMPLICACIONES MÁS ALLÁ DE LA HIPERTENSIÓN / The renin−angiotensin system from circulation to the cell: implications beyond hypertension

The renin-angiotensin system is more complex than was known until recently, since its action is not only limited to the plasma. Its presence has been shown in tissues such as the heart, brain, kidney, pancreas, reproductive system, lymphatic system and adipose tissue, with specific active actions in all of them, and at the same time it is present at the intracellular level of different cell types such as cardiomyocytes and fibroblasts. It is an endocrine, paracrine and autocrine system which is capable of acting at different levels in an independent or related form, taking part not only in the control of blood pressure and homeostasis of water and sodium as initially attributed, but it is also involved in the proper functioning of numerous organs and in the pathophysiological mechanism of structural and func- tional alterations, mainly cardiovascular and renal, which go far beyond hypertension.
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The renin-angiotensin system and its blockers

The renin-angiotensin system and its blockers

Research on the renin-angiotensin system (RAS) has contributed significantly to advances in understand- ing cardiovascular and renal homeostasis and to the treatment of cardiovascular diseases. This review offers a brief history of the RAS with an overview of its major components and their functions, as well as blockers of the RAS, their clinical usage and current research that targets various components of the RAS. Because angiotensin-converting enzyme (ACE) metabolizes two biologically active peptides, one in the kallikrein-kinin system (KKS) and one in the RAS, it is the essential connection between the two systems. ACE releases very powerful hypertensive agent, angiotensin II and also inactivates strong hypotensive peptide, bradykinin. Inhibition of ACE thus has a dual effect, resulting in decreased angiotensin II and increased bradykinin. We described the KKS as well.
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Hemodynamic, morphometric and autonomic patterns in hypertensive rats - renin-angiotensin system modulation

Hemodynamic, morphometric and autonomic patterns in hypertensive rats - renin-angiotensin system modulation

METHODS: Male spontaneously hypertensive rats were randomized into two groups: young (n=13) and adult (n=12). Hemody- namic signals (blood pressure, heart rate), blood pressure variability (BPV) and spectral analysis of the autonomic components of blood pressure were analyzed. LEFT ventricular hypertrophy was measured by the ratio of LV mass to body weight (mg/g), by myocyte diameter (µm) and by relative ibrosis area (RFA, %). ACE and ACE2 activities were measured by luorometry (UF/min), and plasma renin activity (PRA) was assessed by a radioimmunoassay (ng/mL/h). Cardiac gene expressions of Agt, Ace and Ace2 were quantiied by RT-PCR (AU).
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Local Fetal Lung Renin Angiotensin System

Local Fetal Lung Renin Angiotensin System

Effect of PD-123319 treatment on left, right and total lung hypoplasia. Prenatal[r]

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Dissociation between the circulating renin-angiotensin system and angiotensin II receptors in central losartan-induced hypertension

Dissociation between the circulating renin-angiotensin system and angiotensin II receptors in central losartan-induced hypertension

Effects of icv losartan on plasma renin and ACE activity. A group of 16 animals received an icv injection of losartan (90 µg) or isotonic saline and were left in their home cages for 5 min before decapitation. This interval includes the peak pressor response to icv losartan (1,3). Trunk blood was col- lected from each animal into chilled tubes containing either 7.5% EDTA (100 µl/ml) for collection of plasma or gel separator (Becton Dickinson, Plymouth, UK) for col- lection of serum. Plasma was obtained from whole blood centrifuged at 3,000 rpm at 4ºC for 15 min. Plasma and serum were then processed for determination of plasma renin and ACE activity, respectively.
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Effect of race, genetic population structure, and genetic models in two-locus association studies: clustering of functional renin-angiotensin system gene variants in hypertension association studies

Effect of race, genetic population structure, and genetic models in two-locus association studies: clustering of functional renin-angiotensin system gene variants in hypertension association studies

Previous genetic association studies have overlooked the potential for biased results when analyzing different population structures in ethni- cally diverse populations. The purpose of the present study was to quantify this bias in two-locus association studies conducted on an admixtured urban population. We studied the genetic structure distri- bution of angiotensin-converting enzyme insertion/deletion (ACE I/ D) and angiotensinogen methionine/threonine (M/T) polymorphisms in 382 subjects from three subgroups in a highly admixtured urban population. Group I included 150 white subjects; group II, 142 mulatto subjects, and group III, 90 black subjects. We conducted sample size simulation studies using these data in different genetic models of gene action and interaction and used genetic distance calculation algorithms to help determine the population structure for the studied loci. Our results showed a statistically different population structure distribution of both ACE I/D (P = 0.02, OR = 1.56, 95% CI = 1.05-2.33 for the D allele, white versus black subgroup) and angioten- sinogen M/T polymorphism (P = 0.007, OR = 1.71, 95% CI = 1.14- 2.58 for the T allele, white versus black subgroup). Different sample sizes are predicted to be determinant of the power to detect a given genotypic association with a particular phenotype when conducting two-locus association studies in admixtured populations. In addition, the postulated genetic model is also a major determinant of the power to detect any association in a given sample size. The present simula- tion study helped to demonstrate the complex interrelation among ethnicity, power of the association, and the postulated genetic model of action of a particular allele in the context of clustering studies. This information is essential for the correct planning and interpretation of future association studies conducted on this population.
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Renin angiotensin system and cardiac hypertrophy after sinoaortic denervation in rats

Renin angiotensin system and cardiac hypertrophy after sinoaortic denervation in rats

Angiotensins I, II, and 1–7 were quantified in tissue extracts using reverse-phase high-performance liquid chro- matography coupled with ultraviolet (214 nm) detection (HPLC-UV). Peptide separation was accomplished using a 4.6 6 250 mm, 7-mm Aquapore OD 300 column (Applied Biosciences, Foster City, CA), equilibrated with 0.1% phosphoric acid in 5% acetonitrile. The peptides were initially separated by isocratic elution for 5 min, followed by a linear gradient from 5% to 35% acetonitrile in 0.1% phosphoric acid for 20 min at a flow rate of 1.5 mL/min. The left ventriclewas pre-homogenized in 8 mL of 0.1 M sodium phosphate buffer containing 0.34 M sucrose and 0.3 M NaCl (pH 7.2). Angiotensin III (320 ng) was added to each sample as an internal standard. Extraction of angiotensins I, II and 1–7 was achieved using Sep-Pak-C18 column chromatogra- phy (Millipore, Milford, MA). The column was activated with the following steps: 5 mL of methanol, 5 mL of tetrahydrofuran, 5 mL of hexane, 5 mL of methanol, and 10 mL of H 2 O (MilliQ water). The samples were then loaded
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Alternative pathways for angiotensin II generation in the cardiovascular system

Alternative pathways for angiotensin II generation in the cardiovascular system

The classical renin-angiotensin system (RAS) consists of enzymes and peptides that regulate blood pressure and electrolyte and fluid homeostasis. Angiotensin II (Ang II) is one of the most important and extensively studied components of the RAS. The beneficial effects of angiotensin-converting enzyme (ACE) inhibitors in the treatment of hypertension and heart failure, among other diseases, are well known. However, it has been reported that patients chronically treated with effective doses of these inhibitors do not show suppression of Ang II formation, suggesting the involvement of pathways alternative to ACE in the generation of Ang II. Moreover, the finding that the concentration of Ang II is preserved in the kidney, heart and lungs of mice with an ACE deletion indicates the important role of alternative pathways under basal conditions to maintain the levels of Ang II. Our group has characterized the serine protease elastase-2 as an alternative pathway for Ang II generation from Ang I in rats. A role for elastase-2 in the cardiovascular system was suggested by studies performed in heart and conductance and resistance vessels of normotensive and spontaneously hypertensive rats. This mini-review will highlight the pharmacological aspects of the RAS, emphasizing the role of elastase-2, an alternative pathway for Ang II generation.
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Evaluation of renin and angiotensin II levels in pseudoexfoliation syndrome

Evaluation of renin and angiotensin II levels in pseudoexfoliation syndrome

ABSTRACT | Purpose: Pseudoexfoliation syndrome has been linked to impaired function of the heart and blood vessels. We conducted a study to investigate the role of the renin-angiotensin system in the etiopathogenesis of pseudoexfoliation syndrome. Methods: The subjects were 14 patients with pseudoexfoliation syndrome and 14 healthy controls who underwent cataract extraction. Preoperative 5-ml samples of peripheral venous blood and perioperative aqueous humor were collected from the patients in both groups. Plasma and aqueous humor renin levels were analyzed by an immunoradiometric method, and angiotensin II levels were analyzed by radioimmunassay. SPSS version 16.0 was used for statistical analyses. A p-value <0.05 was considered to indicate a statistically significant difference. Results: The mean ages of the patients in pseudoexfoliation and control groups were 71.7 ± 7.1 and 67.4 ± 9.3 years, respectively (p=0.140). The median aqueous humor renin level was 7.73 pg/ml (4.15-21) in the control group and 11.95 pg/ml (3.75-18.54) in pseudoexfoliation group (p=0.022). There were no differences between the two groups in the plasma renin, plasma angiotensin II, or aqueous humor angiotensin II levels. The correlations between plasma and aqueous humor renin levels and between plasma and aqueous humor angiotensin II levels were examined separately for each group; no significant correlations
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Red cell distribution width in relation to incidence of stroke and carotid atherosclerosis: a population-based cohort study.

Red cell distribution width in relation to incidence of stroke and carotid atherosclerosis: a population-based cohort study.

The reason for the association between RDW and mortality is still unknown, and it is un- clear whether RDW is associated with increased incidence of stroke. However, there are several factors that could potentially link RDW to the risk of stroke. For example, activation of the reninangiotensin system leads to increased erythropoiesis and increased RDW.[13] Activa- tion of the reninangiotensin system could also increase the risk of ischemic stroke and intra- cerebral hemorrhage (ICH), for example by increasing the blood pressure.[14,15] Systemic inflammation is related to RDW,[3,4] and is also a risk factor for ischemic stroke.[16] It is not known whether inflammation contributes to hemorrhagic stroke.[16 – 18] One study suggests that RDW is associated with the presence of carotid plaque and carotid intima–media thickness (IMT).[19] If this association remains even after adjustment for cardiovascular risk factors, it could provide one link between RDW and stroke.[20,21]
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