%0 Journal Article
%T ABOUT NOXA, VASCULAR RISK FACTORS, ENDOTHELIAL DYSFUNCTION, AND CONSECUTIVE VASCULOPATHY BUT A LITTLE DIFFERENTLY: HOLISTIC APPROACH OF THE PROBLEM (PRELIMINARY COMMUNICATION)
%A Tam¨¢s Fischer
%J Journal of Pharmaceutical and Scientific Innovation
%D 2013
%I Moksha Publishing House
%X The endothelial system assures unhindered functioning and stability of the internal milieu maintaining vascular health and protecting against vascular injury, noxa. by producing, synthesising and excreting various substances: vasodilators and vasoconstrictors, growth factors and their inhibitors, pro-inflammatory and antiinflammatory agents, pro-thrombotic and fibrinolytic factors, and by keeping them in a strict equilibrium: endothelial dysfunction is the change of these properties, what is inappropriate with regard to the preservation of organ function ("endothelial dysfunction" has been used to define diverse syndromes characterized by changes in distinct endothelial functions, related to a cellular phenotypic switch from a quiescent to an activated state and this multifaceted disorder actually encompasses a spectrum of disturbances in vasomotor responses, antithrombogenic properties, vascular permeability, leukocyte recruitment [inflammation!] and endothelial cell proliferation [remodelling]).In the genesis and later development of chronic vascular injury/vasculopathy (e.g. atherosclerose) endothelial dysfunction (ED) has a crucial key role. The so called risk factors lead to vascular injury through the same mechanism of actions, by inducing oxidative stress (OS ¡ú ED!): Harm (noxa, i.e. isk factors [RFs]) ¡ú oxidative stress [OS] ¡ú endothelial activation [EA], endothlial dysfunction [ED], respectively ¡ú vacular injury, vascular disease). Under physiological conditions free radicals are generated during mitochondrial oxidative metabolism: The walls of the mitochondria are leaky to oxygen radicals produced during metabolism. 1% of oxygen used in respiration actually leaks from the mitochondria in the form of superoxide, but in older subjects, and/or in pathological states, in case of risk facor¡¯s existence (i. e., repeated and/or prolonged mechanical, physical, chemical, microbiological, immunologic, and genetic foreign impacts/disturbing influences/noxious effects!), respectively the proportion is greater: it exposes the cellular constituents to internally generated oxidative attack. As a part of the host defense response, any kind of noxa including the risk factors endangering steadiness of homeostasis start/trigger off an defensive chain founded on increased ROS formation (permanently existing/repeating noxa¡úpersistent/lasting increased ROS formation¡úoxidative stress¡úendothelial activation, endothelial dysfunction, respectively ¡ú |chronic| vascular injury). The difference between normal host defense and detrimental cellular activation may well be a c
%K Endothelial dysfunction
%K oxidative stress
%K risk factors
%K primary and secondary prevention.
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