This study investigated the association of blood pressure with blood oxidative stress-related parameters in normotensive and hypertensive subjects. A cross-sectional design was applied to 31 hypertensive patients and 35 healthy normotensive subjects. All subjects were men between the ages of 35 and 60 years. Exclusion criteria were obesity, dyslipidemia, diabetes mellitus, smoking and current use of any medication. All

Oxidative stress has been associated with mechanisms of EH (essential hypertension). The aim of the present study was to test the hypothesis that the antioxidant properties of vitamins C and E are associated with a decrease in BP (blood pressure) in patients with EH. A randomized double-blind placebo-controlled clinical trial was conducted in 110 men with grade 1 EH (35-60 years of age without obesity, dyslipidaemia and diabetes mellitus, non-smokers, not undergoing vigorous physical exercise, without the use of any medication and/or high consumption of fruit and vegetables). Participants were randomly assigned to receive either vitamins C+E [vitamin C (1 g/day) plus vitamin E (400 international units/day)] or placebo for 8 weeks. Measurements included 24 h ambulatory BP and blood analysis of oxidative-stress-related parameters in erythrocytes (GSH/GSSH ratio, antioxidant enzymes and malondialdehyde) and plasma [FRAP (ferric reducing ability of plasma)], and levels of 8-isoprostane, vitamins C and E were measured at baseline and after treatment. Following administration of vitamins C+E, patients with EH had significantly lower systolic BP, diastolic BP and mean arterial BP and higher erythrocyte and serum antioxidant capacity compared with either placebo-treated patients with EH or the patients with EH at baseline prior to treatment. BP correlated positively with plasma 8-isoprostane levels and negatively with plasma FRAP levels in the vitamins C+E- and placebo-treated groups. In conclusion, the present study supports the view that oxidative stress is involved in the pathogenesis of EH, and that enhancement of antioxidant status by supplementation with vitamins C and E in patients with EH is associated with lower BP. This suggests intervention with antioxidants as an adjunct therapy for hypertension.

Oxidative stress may play a role in the pathogenic mechanism of essential hypertension. Lipid peroxidation can alter the cellular structure of membrane-bound enzymes by changing the membrane phospholipids fatty acids composition. We investigated the relationship between (Na + K)-ATPase activity, lipid peroxidation, and erythrocyte fatty acid composition in essential hypertension. The study included 40 essential hypertensive and 49 healthy normotensive men (ages 35-60 years). Exclusion criteria were obesity, dyslipidemia, diabetes mellitus, smoking, and any current medication. Patients underwent 24-h ambulatory blood pressure monitoring and blood sampling. Lipid peroxidation was measured in the plasma and erythrocytes as 8-isoprostane or malondialdehyde (MDA), respectively. Antioxidant capacity was measured as ferric reducing ability of plasma (FRAP) in the plasma and as reduced/oxidized glutathione (GSH/GSSG ratio) in erythrocytes. (Na + K)-ATPase activity and fatty acids were determined in erythrocyte membranes. Hypertensives had higher levels of plasma 8-isoprostane, erythrocyte MDA, and relative percentage of saturated membrane fatty acids, but lower plasma FRAP levels, erythrocyte GSH/GSSG ratio, (Na + K)-ATPase activity and relative percentage of unsaturated membrane fatty acids, compared with normotensives. Day-time systolic and diastolic blood pressures correlated positively with lipid peroxidation parameters, but negatively with (Na + K)-ATPase activity. These findings suggest that the modulation of (Na + K)-ATPase activity may be associated with changes in the fatty acid composition induced by oxidative stress and provide evidence of a role for this enzyme in the pathophysiology of essential hypertension.

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(Rev Med Chile 2012; 140: 507-511).

Valor del índice de excentricidad del ventrículo izquierdo con tomografía spect de perfusión miocárdica en diversas condiciones. Resumen:Introducción: El índice de excentricidad (IE) obtenido con SPECT miocárdico permite evaluación de esfericidad ventricular izquierda en remodelación patológica.Objetivo: conocer IE en adultos con diversas condiciones cardíacas.Método: Grupo I: Controles (n=44) con >2 factores de riesgo cardiovascular exceptuando Diabetes Mellitus (DM); Grupo II: DM 2 (n=41). Ambos grupos asintomáticos sin enfermedad coronaria conocida. Grupo III: Con alteración de motilidad segmentaria y/o infarto de miocardio (n=64). Grupo IV: Dilatados (n=21) con alteraciones de motilidad difusa o miocardiopatías. Se utilizó Sestamibi-Tc99m y procesamiento QGS. (IE esfera valor ≈0). Resultados Value of left ventricular excentricity index obtained by myocardial perfusion tomography IntroducciónLa remodelación patológica del ventrículo izquierdo es un fenómeno explorado con gran interés en la enfermedad coronaria (EC) debido a su implicancia pronóstica y compleja terapia. Se presenta posterior a infarto de miocardio (IM) como fenómeno compensatorio; también en miocardiopatías, valvulopatías, diversas patologías congénitas e hipertensión pulmonar. El tipo de terapia también tiene efecto sobre el grado de remodelación y de la función ventricular 1,2 . Pacientes con hipertensión arterial pueden presentar remodelación significativa; la disfunción diastólica es un fenómeno asociado y corresponder a una alteración más precoz 3 . Específicamente, en el IM la pérdida aguda de tejido miocárdico, de otras células y de la matriz extracelular ocasiona un abrupto incremento en las condiciones de estrés que induce una forma particular de remodelación en la zona infartada misma y en el miocardio distante, que además contribuye a la generación de disfunción ventricular y dilatación progresiva del ventrículo. Los mecanismos involucrados en la remodelación patológica son complejos e incluyen diversos factores de activación neurohormonales, de inflamación, de necrosis, así como de estrés oxidativo con alteraciones a nivel de miocitos, de fibroblastos, de otras células, así como del colágeno y de otros componentes de la matriz extracelular. Existen alteraciones fenotípicas involucradas; por ejemplo, se ha descrito recientemente fibrosis miocárdica como manifestación temprana de miocardiopatía hipertrófica. El estado profibrótico en pacientes con mutaciones de sarcómero mostraron biomarcadores de colágeno más elevados que en controles asociado a alteraciones en resonancia magné-tica (RM) cardíaca 4 . La revascularización coronaria mejora los fenómenos de remodelación, lo que se asocia a recuperación de función ventricular, evaluada con parámetros sistólicos: fracción de eyección ventricular izquierda (FEVI) y volúmenes 5 . Es importante mencionar que posterior a un IM la apertura de la arteria culpable disminuye la remodelación patológica 6 . La angioplastía primaria post IM disminuye la alteración de la contractilidad regional, p...

La inflamación en la hipertensión arterial, mecanismos de producción e implicancias terapéuticashernán prat 1* , patriCio araoS 2,a* , lUiS MiChea 3,4,5 role of inflammation in hypertensionEven though the mechanisms that mediate essential hypertension (HT) are not fully understood, an immunological-inflammatory mechanism could be the common pathway for diverse pathophysiological mechanisms. We analyze in a simplified way the participation of the immune system in HT. T lymphocytes (TL) and antigen presenting cells (APCs) are components of the immune system capable of generating proinflammatory cytokines. They cause endothelial damage, vasoconstriction, and decreased urinary sodium excretion. CD4+ and CD8+ TL are effector cells, causally implicated in the development of HT, whereas type γδ TL play their pathogenic role in HT enhancing endothelial dysfunction. Additionally, a immunomodulation decrease by regulatory TL, worsens endothelial dysfunction and reduces vasodilation in experimental HT. Results of recent studies indicate that lymphocyte activation would be mediated by antigens captured by antigen APCs for subsequent presentation to "naive" TL. On the other hand, proinflammatory states such as obesity, the change of the intestinal microbiota and the increase in salt intake favors TL and APC activation, contributing to HT development.