[Frontiers in Bioscience S3, 946-960, June 1, 2011]
Endothelial dysfunction in hypertension: The role of arginase
Danielle L Michell1,2, Karen L Andrews1, Jaye PF Chin-Dusting1
1Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia. 2Department of Medicine Alfred Hospital, Monash University, Melbourne, Victoria, Australia
TABLE OF CONTENTS
Essential hypertension is the leading risk factor for mortality worldwide, accountable for 13% of deaths globally. Despite numerous therapies available uncontrolled hypertension is still very prevalent today and a large subset are shown to have treatment resistant hypertension. Several cardiovascular diseases including hypertension result in endothelial dysfunction and inflammation. Once thought of as a passive barrier between blood flow and tissue the endothelium is now considered a main hub for maintaining vascular tone, structure and haemostasis. Several pathways occur in the endothelium that can result in dysfunction and altered vascular stasis. Such pathways include the impairment of the vasodilator nitric oxide (NO), increases in pro-inflammatory pathways such as ROS (reactive oxygen species) production and also recent reports suggest that the enzyme arginase, associated with the L-arginine-urea cycle, may be an important factor that is increased in hypertension. These pathways may offer alternative mechanisms to treat the complications associated with hypertension rather than the conventional therapies that aim to lower blood pressure.