[Stroke and renin-angiotensin system].
Angiotensin II is a key mediator in the mechanism of hypertension and plays a pathophysiological role for the development of ischemic stroke. Activation of AT1 receptors by angiotensin II initiates a complex signaling cascade via in part reactive oxygen species produced by the enzyme NADPH oxidase in blood vessels and induces vasoconstriction, vascular proliferation, and inflammation leading to cerebrovascular insufficiency. On the other hand, AT2 receptors are potentially protective. Recently, many clinical trials showed inhibition of renin-angiotensin system(AT1 receptor blockers and ACE inhibitors) has beneficial effect on stroke prevention independent of blood pressure lowering. Inhibition of renin-angiotensin system is a new promising strategy for stroke prevention.
Tanahashi
Norio
N
Department of Neurology, Saitama Medical School.
D000804:Angiotensin II / Q000502:physiology; D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000818:Animals; D002986:Clinical Trials as Topic; D006801:Humans; D019255:NADPH Oxidases / Q000502:physiology; D017382:Reactive Oxygen Species / Q000378:metabolism; D044140:Receptor, Angiotensin, Type 1 / Q000378:metabolism; D012084:Renin-Angiotensin System / Q000502:physiology*; D020521:Stroke / Q000209:etiology* / Q000517:prevention & control*
D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors; D017382:Reactive Oxygen Species; D044140:Receptor, Angiotensin, Type 1; D000804:Angiotensin II; D019255:NADPH Oxidases