High blood pressure, oxygen radicals and antioxidants: etiological relationships.
This hypothesis proposes that high blood pressure is a pathological state associated with a loss of the balance between pro-oxidation and antioxidation, energy depletion, and accelerated aging in the target organs, such as heart, kidney and brain. Different nutritional, environmental, pharmacological factors and/or associated pathologies (diabetes, arteriosclerosis, cancer, alcoholism, etc.) and/or genetic components, can induce high blood pressure by breaking the redox equilibrium in the affected organs. Additional evidence, such as increase of oxidative damage, fibrogenesis, inhibition of the cardiocytic sodium-potassium pump, and heart hypertrophy, supports this hypothesis. These facts are analysed in the present paper, showing that they could contribute to the development of high blood pressure and associated pathologies by oxidative mechanisms.
Romero-Alvira
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Residencia General de la Seguridad Social, Hospital Miguel Servet, Zaragoza, Spain.
Roche
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E
D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001794:Blood Pressure / Q000502:physiology; D006332:Cardiomegaly / Q000150:complications; D000431:Ethanol / Q000009:adverse effects; D005355:Fibrosis; D006801:Humans; D006973:Hypertension / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D008955:Models, Cardiovascular; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism; D012307:Risk Factors; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors
D000975:Antioxidants; D017382:Reactive Oxygen Species; D000431:Ethanol; D000254:Sodium-Potassium-Exchanging ATPase