Abstract
PURPOSE OF REVIEW: To review recent data that suggest opposing effects of brain angiotensin type-1 (AT(1)R) and type-2 (AT(2)R) receptors on blood pressure (BP). Here, we discuss recent studies that suggest pro-hypertensive and pro-inflammatory actions of AT(1)R and anti-hypertensive and anti-inflammatory actions of AT(2)R. Further, we propose mechanisms for the interplay between brain angiotensin receptors and neuroinflammation in hypertension. RECENT FINDINGS: The renin-angiotensin system (RAS) plays an important role in regulating cardiovascular physiology. This includes brain AT(1)R and AT(2)R, both of which are expressed in or adjacent to brain regions that control BP. Activation of AT(1)R within those brain regions mediate increases in BP and cause neuroinflammation, which augments the BP increase in hypertension. The fact that AT(1)R and AT(2)R have opposing actions on BP suggests that AT(1)R and AT(2)R may have similar opposing actions on neuroinflammation. However, the mechanisms by which brain AT(1)R and AT(2)R mediate neuroinflammatory responses remain unclear. The interplay between brain angiotensin receptor subtypes and neuroinflammation exacerbates or protects against hypertension.