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

Abstract:

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.

journal_name

Curr Hypertens Rep

authors

Satou R,Penrose H,Navar LG

doi

10.1007/s11906-018-0900-0

subject

Has Abstract

pub_date

2018-10-05 00:00:00

pages

100

issue

12

eissn

1522-6417

issn

1534-3111

pii

10.1007/s11906-018-0900-0

journal_volume

20

pub_type

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