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- W2894807585 abstract "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.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." @default.
- W2894807585 created "2018-10-12" @default.
- W2894807585 creator A5004907690 @default.
- W2894807585 creator A5007394438 @default.
- W2894807585 creator A5036635132 @default.
- W2894807585 date "2018-10-05" @default.
- W2894807585 modified "2023-10-14" @default.
- W2894807585 title "Inflammation as a Regulator of the Renin-Angiotensin System and Blood Pressure" @default.
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