Malfunction of vascular control in lifestyle-related diseases: oxidative stress of angiotensin II-induced hypertension: mitogen-activated protein kinases and blood pressure regulation.
The candidate mechanisms 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 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.
Kimura
Shoji
S
Department of Pharmacology, Kagawa University Medical School, Kagawa 761-0793, Japan. kimura@kms.ac.jp
Zhang
Guo-Xing
GX
Abe
Youichi
Y
D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D001794:Blood Pressure; D004789:Enzyme Activation; D006801:Humans; D006973:Hypertension / Q000209:etiology* / Q000378:metabolism; D020928:Mitogen-Activated Protein Kinases / Q000502:physiology*; D019255:NADPH Oxidases / Q000378:metabolism; D018384:Oxidative Stress; D051381:Rats; D014661:Vasoconstriction / Q000187:drug effects
D000804:Angiotensin II; D019255:NADPH Oxidases; D020928:Mitogen-Activated Protein Kinases