Malfunction of Vascular Control in Lifestyle-Related Diseases: Oxidative Stress of Angiotensin II-induced Hypertension: Mitogen-Activated Protein Kinases and Blood Pressure Regulation

Malfunction of Vascular Control in Lifestyle-Related Diseases: Oxidative Stress of Angiotensin II-induced Hypertension: Mitogen-Activated Protein Kinases and Blood Pressure Regulation

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The candidate mechanisms Shock Sensor for maintaining hypertension in a chronically angiotensin II (Ang II)-infused state include direct vasoconstriction of the vasculature, disturbance of renal water/sodium handling, and central/peripheral sympathetic nerve regulation of hemodynamics.The involvement of reactive oxygen species (ROS) has been studied in these proposed mechanisms and the importance of ROS in progression of Ang II-induced hypertension has been accepted.We recently reported ROS-sensitive blood pressure regulation in chronically as well as acutely Ang II-infused hypertensive rats.The facts suggested that mechanisms for maintaining high peripheral vascular resistance in chronically Ang II-infused hypertensive rats were different from 24" Double Wall Oven those involved in the acute hypertensive response to Ang II from the perspective of ROS sensitivity and that there must be a time-dependent transition from ROS-non-sensitive to ROS-sensitive vasoconstriction during prolonged Ang II infusion.

In this review, we introduced our recent work describing the time transition of ROS sensitivity in Ang II-induced hypertension and activation of cardiovascular mitogen-activated protein kinase (MAPK) in acute and chronic phases Ang II infusion in conscious rats.Keywords:: angiotensin, vasoconstriction, tempol, superoxide anion, mitogen-activated protein kinase.