Inflammation as a Regulator of the Renin-Angiotensin System and Blood Pressure

• Published in: Current hypertension reports Vol. 20; no. 12; pp. 100 - 9
• Main Authors: Satou, Ryousuke, Penrose, Harrison, Navar, L. Gabriel
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.12.2018; Springer Nature B.V
• Subjects: Blood pressure; Cardiology; Cytokines; Family Medicine; General Practice; Hypertension; Immune system; Internal Medicine; Mechanisms of Hypertension (M Weir; Medicine; Medicine & Public Health; Metabolic Diseases; Nephrology; Primary Care Medicine; Section Editor; Topical Collection on Mechanisms of Hypertension; Hypertension; Inflammation; The renin-angiotensin system; Intracellular signaling
• ISSN: 1522-6417; 1534-3111
• DOI: 10.1007/s11906-018-0900-0

Purpose of Review Mechanisms facilitating progression of hypertension via cross stimulation of the renin-angiotensin system (RAS) and inflammation have been proposed. Accordingly, we review and update evidence for regulation of RAS components by pro-inflammatory factors. Recent Findings Angiotensin II (Ang II), which is produced by RAS, induces vasoconstriction and consequent blood pressure elevation. In addition to this direct action, chronically elevated Ang II stimulates several pathophysiological mechanisms including generation of oxidative stress, stimulation of the nervous system, alterations in renal hemodynamics, and activation of the immune system. In particular, an activated immune system has been shown to contribute to the development of hypertension. Recent studies have demonstrated that immune cell-derived pro-inflammatory cytokines regulate RAS components, further accelerating systemic and local Ang II formation. Specifically, regulation of angiotensinogen (AGT) production by pro-inflammatory cytokines in the liver and kidney is proposed as a key mechanism underlying the progression of Ang II-dependent hypertension.