Brain Angiotensin Type-1 and Type-2 Receptors in Physiological and Hypertensive Conditions: Focus on Neuroinflammation
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SECONDARY HYPERTENSION: NERVOUS SYSTEM MECHANISMS (M WYSS, SECTION EDITOR)
Brain Angiotensin Type-1 and Type-2 Receptors in Physiological and Hypertensive Conditions: Focus on Neuroinflammation Khalid Elsaafien 1 & Annette D. de Kloet 2,3,4 & Eric G. Krause 1,3,4 & Colin Sumners 2,3,4
# Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Purpose of Review To review recent data that suggest opposing effects of brain angiotensin type-1 (AT1R) and type-2 (AT2R) receptors on blood pressure (BP). Here, we discuss recent studies that suggest pro-hypertensive and pro-inflammatory actions of AT1R and anti-hypertensive and anti-inflammatory actions of AT2R. 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 AT1R and AT2R, both of which are expressed in or adjacent to brain regions that control BP. Activation of AT1R within those brain regions mediate increases in BP and cause neuroinflammation, which augments the BP increase in hypertension. The fact that AT1R and AT2R have opposing actions on BP suggests that AT1R and AT2R may have similar opposing actions on neuroinflammation. However, the mechanisms by which brain AT1R and AT2R mediate neuroinflammatory responses remain unclear. Summary The interplay between brain angiotensin receptor subtypes and neuroinflammation exacerbates or protects against hypertension. Keywords Brain angiotensin receptors . AT1R . AT2R . Neuroinflammation . Microglia . Hypertension
Introduction The renin-angiotensin system (RAS) plays an important regulatory role in cardiovascular physiology [1]. This involves the actions of angiotensin II (Ang II) on angiotensin II type 1 (AT1R) and type 2 (AT2R) receptors within or near the brain cardiovascular control centers [2, 3]. AT1R-mediated effects This article is part of the Topical Collection on Secondary Hypertension: Nervous System Mechanisms * Colin Sumners [email protected] 1
Department of Pharmacodynamics, University of Florida College of Pharmacy, Gainesville, FL, USA
2
Department of Physiology and Functional Genomics, College of Medicine, University of Florida, Gainesville, FL, USA
3
Center for Integrative Cardiovascular and Metabolic Diseases, University of Florida, Gainesville, FL, USA
4
Evelyn F. and William L. McKnight Brain Institute, University of Florida, Gainesville, FL, USA
of Ang II within those centers result in sympatho-excitaion and vasopressin and corticosterone secretion, leading to increases in blood pressure (BP) [4–6, 7••]. Importantly, those mechanisms contribute to neurogenic hypertension, which is characterized by chronic sympatho-excitation [8, 9]. On the other hand, brain AT2R are thought to elicit opposing effects to AT1R [10, 11•, 12] and are suggested to be protective against hypertension [3]. AT2R-mediated effects of Ang II result in sympatho-inhibition and attenuate vasopressin
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