Salt feedback on the renin-angiotensin-aldosterone system

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.

Angiotensin II regulates phosphorylation of actin‐associated proteins in human podocytes

“…Generation and characterization of stably transfected AB8 3F-AT1R cell lines has been previously described (14). For relative quantification of the phosphoproteome, AB8 3F-AT1R podocytes were grown in stable isotope labeling with amino acids in cell culture (SILAC) (16) 4 arginine, [ 12 C] 6 lysine) for 3 passages. This labeling period is sufficient to achieve .98% saturation of labeling (17).…”

“…The peptide hormone, angiotensin II (AngII), is a major component of the renin-angiotensin-aldosterone system (RAAS) and, thus, a crucial regulator of blood pressure, salt-water balance, sympathetic nervous system, and tissue homeostasis (4). AngII mediates the vasoconstriction of the efferent glomerular arteriole, thereby physiologically regulating the glomerular filtration rate (5).…”

A Single Urine Sodium Measurement May Validly Estimate 24‐hour Urine Sodium Excretion in Patients With an Ileostomy

“…Renal sodium and fluid excretion normally reflects dietary intake . A decrease in sodium intake increases renin synthesis, which initiates the renin‐angiotensin‐aldosterone system . Aldosterone increases the number of active epithelial sodium channels in the distal nephron and collecting tubules and thereby participates in sodium balance regulation by increasing the renal sodium reabsorption .…”

Role of the alternative splice variant of NCC in blood pressure control

“…In response to water loading, a strong decrease in expression of NCC 3 as well as NCC SV was shown [20]. Water loading results in transient extracellular volume expansion and decrease in serum osmolality, which is known to deactivate RAAS and reduce AVP release [76]. AVP is mainly known for its water-retaining action on collecting duct (CD) by increasing the abundance of the water channel aquaporin 2 (AQP2) [77].…”