Abstract
Sustained Hypertension (HT) causes atherosclerotic changes and is one of the main risk factor of coronary artery disease. It is not clear if White Coat Hypertension (WCH) also causes atherosclerosis as it is associated with other target organ changes similar to those with sustained SHT. It is well established that in sustained HT the process of endothelial damage and angiogenesis are abnormal. The relationship of oxidative stress and nitric oxide (NO) is well known.The low level of NO in WCH may be the result of enhanced oxidative stress. Increased oxidative stress is probably the leading cause of endothelial dysfunction. In consecutive studies, we investigated arterial compliance and analyzed the molecules produced by endothelial cells by biochemical methods to determine endothelial dysfunction. Increasing of oxidative products (oxidative modification of low-density lipoprotein -oxLDL- and malondialdehyde -MDA-) showed the enhanced oxidative stress while the low levels of antioxidants (paraoxonase -PON1-) denoted the decrease in antioxidant activity. The decrease in endothelium dependent flow mediated dilatation and elevated plasma levels of the endogenous (NO) synthase inhibitor asymmetric dimethyl arginine (ADMA), increases in endothelin (ET-1), homocysteine and vascular endothelial growth factor (VEGF) may contribute to endothelial dysfunction and abnormal angiogenesis in WCH. The data and our current findings were discussed to assess the increased cardiovascular risk in WCH conferred by endothelial dysfunction and high oxidative stress. As the elevated oxidative stres is a strong risk factor for coronary artery disease WCH might not be considered as an innocent trait.
Keywords: White coat hypertension, endothelial dysfunction, NO, ADMA, ET-1, VEGF
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