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Mineralocorticoid-induced sodium appetite and renal salt retention: evidence for
common signaling and effector mechanisms
#MMPMID25376899
Fu Y
; Vallon V
Nephron Physiol
2014[]; 128
(1-2
): 8-16
PMID25376899
show ga
An increase in renal sodium chloride (salt) retention and an increase in sodium
appetite are the body's responses to salt restriction or depletion in order to
restore salt balance. Renal salt retention and increased sodium appetite can also
be maladaptive and sustain the pathophysiology in conditions like salt-sensitive
hypertension and chronic heart failure. Here we review the central role of the
mineralocorticoid aldosterone in both the increase in renal salt reabsorption and
sodium appetite. We discuss the working hypothesis that aldosterone activates
similar signaling and effector mechanisms in the kidney and brain, including the
mineralocorticoid receptor, the serum- and glucocorticoid-induced kinase SGK1,
the ubiquitin ligase NEDD4-2, and the epithelial sodium channel ENaC. The latter
also mediates the gustatory salt sensing in the tongue, which is required for the
manifestation of increased salt intake. Effects of aldosterone on both the brain
and kidney synergize with the effects of angiotensin II. Thus, mineralocorticoids
appear to induce similar molecular pathways in the kidney, brain, and possibly
tongue, which could provide opportunities for more effective therapeutic
interventions. Inhibition of renal salt reabsorption is compensated by
stimulation of salt appetite and vice versa; targeting both mechanisms should be
more effective. Inhibiting the arousal to consume salty food may improve a
patient's compliance to reducing salt intake. While a better understanding of the
molecular mechanisms is needed and will provide new therapeutic options, current
pharmacological interventions that target both salt retention and sodium appetite
include mineralocorticoid receptor antagonists and potentially inhibitors of
angiotensin II and ENaC.
|Aldosterone/*metabolism
[MESH]
|Angiotensin II/metabolism
[MESH]
|Animals
[MESH]
|Appetite/physiology
[MESH]
|Blood Pressure/physiology
[MESH]
|Epithelial Sodium Channels
[MESH]
|Humans
[MESH]
|Hypertension/etiology/metabolism
[MESH]
|Kidney/physiology
[MESH]
|Mineralocorticoid Receptor Antagonists/therapeutic use
[MESH]
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