Target organ damage in hypertension: Pathophysiology and implications for drug therapy

Sunil K. Nadar, Muzahir H. Tayebjee, Franz Messerli, Gregory Y.H. Lip*

*المؤلف المقابل لهذا العمل

نتاج البحث: المساهمة في مجلةReview articleمراجعة النظراء

64 اقتباسات (Scopus)


Hypertension is a well known risk factor for cardiovascular and cerebrovascular events such as heart attacks and strokes. In addition, it is associated with earlier changes in organ systems in the body, such as left ventricular hypertrophy (LVH), proteinuria and renal failure, retinopathy and vascular dementia which are grouped under the term "target organ damage"(TOD). There are many processes involved in the pathogenesis of TOD and these include endothelial activation, platelet activation, increased thrombogenesis, changes in the renin aldosterone angiotensin system (RAAS), and collagen turnover. All these changes work hand in hand and lead to the production of hypertensive TOD. In this review, we aim to provide an overview of the recent advances in pathophysiology of hypertensive TOD, and examine how these changes lead to the production of TOD. A better understanding of these pathogenic processes would help us better devise treatment strategies in preventing the dreaded complications associated with hypertension.

اللغة الأصليةEnglish
الصفحات (من إلى)1581-1592
عدد الصفحات12
دوريةCurrent Pharmaceutical Design
مستوى الصوت12
رقم الإصدار13
المعرِّفات الرقمية للأشياء
حالة النشرPublished - مايو 2006
منشور خارجيًانعم

ASJC Scopus subject areas

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