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Pflugers Arch - Eur J Physiol (2015) 467:565576 DOI 10.1007/s00424-014-1668-y
INVITED REVIEW
Salt feedback on the renin-angiotensin-aldosterone system
Frank Schweda
Received: 15 October 2014 /Revised: 2 December 2014 /Accepted: 2 December 2014 /Published online: 13 December 2014 # Springer-Verlag Berlin Heidelberg 2014
Abstract The renin-angiotensin-aldosterone system (RAAS) is a central element in the control of the salt and water balance of the body and arterial blood pressure. The activity of the RAAS is controlled by the protease renin, which is released from renal juxtaglomerular epithelioid cells (JGE cells) into the circulation. Renin release is regulated by a complex interplay of several locally acting hormones or mechanisms and longer feedback loops one of which involves salt intake. Acute NaCl loads or longer lasting high salt intakes suppress plasma renin activity, whereas reductions in NaCl intake stimulate it. Because the activation of the RAAS conserves the salt content of the body, a classical feedback loop between salt intake/body salt content and renin is established. Despite of its important role for body fluid homeostasis, the precise signaling pathways connecting salt intake with the synthesis and release of renin are only incompletely understood. Four putative controllers of the salt-dependent regulation of the RAAS have been suggested: (1) the macula densa mechanism which adjusts renin release in response to changes in the renal tubular salt concentration; (2) salt-dependent changes in the arterial blood pressure; (3) circulating salt-dependent hormones, particularly the atrial natriuretic peptide (ANP); and(4) renal sympathetic nervous activity, which is regulated by extracellular volume and arterial blood pressure. In this review, the role of these known controllers of the RAAS will be discussed with special emphasis on their relative contributions to the salt-dependent regulation of the RAAS at different time frames.
Keywords Renin . Renin-angiotensin system . Salt intake . Salt load
Introduction
Since the discovery of renin more than a century ago, numerous studies have dealt with its biological actions and the regulation of its synthesis and release. Renin is an aspartyl protease that is released from the juxtaglomerular epithelioid cells (JGE cells) into the circulation, where it cleaves the peptide angiotensin I (angI) from liver-derived angiotensinogen (Fig. 1). In turn, angI is converted into angiotensin II (angII) by the angiotensin-converting enzyme (ACE). AngII is the main effector...