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Oxidative Stress and Endothelial Dysfunction in White Coat Hypertension: Data of the Group from Cerrahpasa Medical Faculty | OMICS International | Abstract
ISSN: 2167-1095

Journal of Hypertension: Open Access
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Review Article

Oxidative Stress and Endothelial Dysfunction in White Coat Hypertension: Data of the Group from Cerrahpasa Medical Faculty

Yesari Karter*

Department of Internal Medicine, Cerrahpasa Faculty of Medicine, Istanbul University, 34303 Cerrahpasa- Istanbul, Turkey

*Corresponding Author:
Yesari Karter
Department of Internal Medicine
Cerrahpasa Faculty of Medicine
Istanbul University, 34303 Cerrahpasa- Istanbul, Turkey
Tel: 90 212 414 30 00
Fax: 90 212 414 35 96
E-mail: [email protected]

Received Date: May 31, 2014; Accepted Date: July 28, 2014; Published Date: August 1, 2014

Citation: karter Y (2014) Oxidative Stress and Endothelial Dysfunction in White Coat Hypertension: Data of the Group from Cerrahpasa Medical Faculty. J Hypertens 3:163 doi:10.4172/2167-1095.1000163

Copyright: © 2014 karter Y. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


In 2000 a group of authors from Ä°stanbul University CerrahpaÅŸa Medical Faculty Internal Medicine Department interesting in hypertension (HT) especially White Coat Hypertension (WCH) come together and began to study on WCH. We founded a team and act as a referral center in our faculty.

Cases with blood pressure >140-90 were referred to our clinic. We classified the cases into sustained hypertension (HT) and white coat hypertension (WCH) groups. We defined WCH as clinical hypertension and day time ambulatory blood pressure less than 135/85.

First of all we investigated if WCH were innocent. With this purpose we searched for the target organ damage with a cross sectional study and our manuscript was published (Target organ damage and change in arterial compliance). We studied the metabolic changes caused by WCH and it was also published within the same manuscript.

Since that time we have been following up these groups longitudinally to see if WCH turns to sustained HT or target organ damage and/or metabolic changes occur by the time. We are planning to report the progression of twenty years in 2020.

It has been documented that oxidative stress and endothelial dysfunction participated in the pathogenesis of sustained hypertension. As we observed white coat is not innocent due to our previous studies we aimed to see if there also exists oxidative stress and endothelial dysfunction in WCH with some serial studies using different markers such as asymmetric dimethyl arginine (ADMA) a competitive inhibitor of NO (nitric oxide), homocystein (decreasing the bioavailibity of NO), paroxanase (PON; preventing lipid oxidation), oxLDL, sLOX-1 (oxidation products of lipids and proteins) and endogenous antioxidan components. It has been observed that the majority of our studies evaluating endothelial function indicated that endothelial dysfunction is more prevalent in WCH than in NT, but it is either equal or worse in HT as compared to WCH.


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