CHF: Circulatory Homeostasis Gone Awry

Abstract

The role of the renin-angiotensin-aldosterone system (RAAS) is integral to salt and water retention, particularly by the kidneys. Over time, positive sodium balance leads first to intra- and then to extravascular volume expansion, with subsequent symptomatic heart failure. This report examines the role of the RAAS in regulating a less well recognized component essential to circulatory homeostasis--central blood volume. The regulation of central blood volume draws on integrative cardiorenal physiology and a key role played by the RAAS in its regulation. In presenting insights into the role of the RAAS in regulating central blood volume, this review also addresses other sodium-retaining states with a predisposition to edema formation, such as cirrhosis and nephrosis.

Mechanisms in fluid retention – towards a mutual concept

“…Traditionally, initiation of compensatory systems in heart failure has been regarded as a response to diminished stimulation of high‐pressure baroreceptors due to a functional arterial underfilling leading to activation of SNS and decreased tissue perfusion notably in the kidneys leading to activation of RAAS (Weber et al , ; Lee & Tkacs, ; Dube & Weber, ; Florea & Cohn, ). However, other initiators of compensatory mechanisms in heart failure have been proposed such as systemic microvascular endothelial inflammation due to already existing conditions leading to myocardial fibrosis as well as remodelling of left ventricle due to hypertension (Davila et al , ; Redfield, ).…”