Hypertension, angiotensin, and stroke: beyond blood pressure.

Abstract

Hypertension (HTN) is a major risk factor for all stroke subtypes, infarction as well as hemorrhage.1,2 Evidence from clinical trials shows that control of blood pressure (BP) leads to a substantially lower risk of stroke.3 HTN exerts detrimental actions on the cerebral circulation that play a critical role in its ability to promote cerebrovascular diseases. Angiotensin II (Ang II) is a key mediator by which HTN exerts its deleterious vascular effects. Recent findings raise the possibility that some of the detrimental actions of Ang II are independent of the associated elevation in BP. Here we will discuss the effect of HTN on stroke in light of recent advances indicating that the renin angiotensin system (RAS) may a play a role greater than previously believed in the deleterious cerebrovascular actions of HTN and, as such, is a promising target for stroke prevention. HTN is the most prevalent and powerful modifiable risk factor for stroke, irrespective of geographic region and ethnic group.1,4 Persons with HTN are about 3 or 4 times more likely to have a stroke.2 Whereas diastolic BP was once thought to be the most important predictor of stroke, the relationship between stroke and HTN may be stronger for systolic than for diastolic BP.5 The association between BP and stroke risk seems to occur on a continuum rather than as a threshold effect.6 The majority of strokes have been reported among persons with only “borderline” or “mild” HTN, and both persons classified as “hypertensive” as well as “normotensive” may benefit from BP lowering. Therefore, although the highest BP levels predict the highest relative risk of stroke, the conceptual pendulum has swung in the direction of the continuum of absolute BP levels and somewhat away from the construct of “hypertension” per se. Furthermore, as discussed …