ABSTRACT
A disfunção endotelial atua tanto na aterogênese como na precipitação das síndromes coronárias agudas. A redução da biodisponibilidade do óxido nítrico é expressão de endotélio disfuncional. O mecanismo desta redução não está elucidado. A presença de disfunção endotelial foi correlacionada com fatores de risco (FR), nitrato sanguíneo e fatores genéticos (polimorfismo do óxido nítrico sintase endotelial / The endothelial dysfunction plays an important roll in the atherogenesis and precipitation of acute coronary syndromes. The reduction of bioavailability of the nitric oxide is the expression of endothelial dysfunction. The exact mechanism of this reduction is not yet well explained. In order to evaluate the presence of endothelial dysfunction and correlation with risk factors (FR), nitrate blood levels and genetic factors (endothelial nitric oxide syntethase polymorphism, fibrinogen and PAI-1) a 128 myocardial infarction patients group with age ≤ 40 year was studied, and underwent a brachial artery ultra-sound. The results were compared with a group of young health individuals...
Subject(s)
Adult , Endothelium/physiopathology , Endothelium-Dependent Relaxing Factors/analysis , Vasodilation/physiology , Brachial Artery , Vasodilation/genetics , Nitric Oxide/geneticsABSTRACT
The present study was designed to examine blood pressure response to nitric oxide synthase-pathway inhibition and stimulation in normotensive and hypertensive diabetic rats. Rats treated with streptozotocin (60 mg/Kg ip) developed high blood glucose, polyuria and slow weight gain compared with control. One group of diabetic rats developed hypertension, consequently we studied three experimental groups: control rats (C), normotensive diabetic rats (ND) and hypertensive diabetic rats (HD). Mean arterial pressure (MAP), systolic blood pressure, diastolic blood pressure and heart rate were recorded: baseline time, 30'after L-nitro arginine methyl ester (L-NAME: 1 mg/Kg iv) and post L-arginine (L-arg: 250 mg/Kg iv) injection. L-NAME induced a significantly increase in MAP in all groups. This enhancement was smaller in diabetic than in control rats. The increase in MAP in HD was significantly lower than that in NDL-arg induced a significantly decrease in MAP in all groups. This decrease was significantly attenuated in diabetic compared with control rats. The degree of hypotension in response to L-arg in diabetic groups was lower in hypertensive than that in normotensive diabetic rats. These data suggest that an impairment of nitric oxide formation could be involved in the development of hypertension in this model.
Subject(s)
Animals , Male , Rats , Arginine/analogs & derivatives , Arginine/pharmacology , Blood Pressure/drug effects , Diabetes Mellitus, Experimental/physiopathology , Enzyme Inhibitors/pharmacology , Hypertension/physiopathology , NG-Nitroarginine Methyl Ester/pharmacology , Nitric Oxide/antagonists & inhibitors , Analysis of Variance , Endothelium, Vascular/drug effects , Endothelium-Dependent Relaxing Factors/analysis , Hemodynamics , Rats, Wistar , StreptozocinABSTRACT
En la última década se ha podido establecer que el Oxido Nítrico (ON) corresponde al llamado Factor Relajante Derivado del Endotelio, dado que mediante el uso de inhibidores competitivos del ON se inducía contracción vascular, efecto revertido por el tratamiento con L-arginina, precursor de la biosíntesis del ON, mediada ésta por la acción de la ON Sintetasa. El ON ha sido implicado entre muchos aspectos, en la generación de daño tisular y patogénesis de algunas condiciones vasculares como vasoespasmo, ateroesclerosis, diabetes mellitus, hipertensión esencial y preeclampsia; de igual forma han sido planteadas novedosas aplicaciones de la inhibición de la ON Sintetasa en el enfoque terapéutico de la inflamación y el shock