Key result
High salt intake increased renal fibrosis 2.2-fold in 5/6-nephrectomized rats compared to low salt, an effect reduced by central renin-angiotensin blockade or renal denervation (all P<0.05).
Why the study?
Does a high-salt diet promote CKD progression via a reno-cerebral reflex activating the renin-angiotensin system in 5/6-nephrectomized rats?
Does a high-salt diet promote CKD progression via a reno-cerebral reflex activating the renin-angiotensin system in 5/6-nephrectomized rats?
High salt intake promotes CKD progression independent of blood pressure via a reno-cerebral reflex that activates the renin-angiotensin system.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for reno-cerebral reflex in salt-sensitive CKD models; leaves open human relevance and requires prospective validation.
Salt intake promotes progression of CKD by uncertain mechanisms. We hypothesized that a salt-induced reno-cerebral reflex activates a renin-angiotensin axis to promote CKD. Sham-operated and 5/6-nephrectomized rats received a normal-salt (0.4%), low-salt (0.02%), or high-salt (4%) diet for 2 weeks. High salt in 5/6-nephrectomized rats increased renal NADPH oxidase, inflammation, BP, and albuminuria. Furthermore, high salt activated the intrarenal and cerebral, but not the systemic, renin-angiotensin axes and increased the activity of renal sympathetic nerves and neurons in the forebrain of these rats. Renal fibrosis was increased 2.2-fold by high versus low salt, but intracerebroventricular tempol, losartan, or clonidine reduced this fibrosis by 65%, 69%, or 59%, respectively, and renal denervation or deafferentation reduced this fibrosis by 43% or 38%, respectively (all P<0.05). Salt-induced fibrosis persisted after normalization of BP with hydralazine. These data suggest that the renal and cerebral renin-angiotensin axes are interlinked by a reno-cerebral reflex that is activated by salt and promotes oxidative stress, fibrosis, and progression of CKD independent of BP.
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Cao et al. (2015) studied CKD. High-salt diet vs. Normal-salt (0.4%) or low-salt (0.02%) diet was evaluated on Renal fibrosis (2.2-fold increase, p=<0.05). High salt intake increased renal fibrosis 2.2-fold in 5/6-nephrectomized rats compared to low salt, an effect reduced by central renin-angiotensin blockade or renal denervation (all P<0.05).
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