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An unexpected role for angiotensin II in the link between dietary salt and proximal reabsorption
/articles/view/26092
Published April 3, 2006
Citation Information: J Clin Invest. 2006;116(4):1110-1116. https://doi.org/10.1172/JCI26092.
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Research Article Nephrology

An unexpected role for angiotensin II in the link between dietary salt and proximal reabsorption

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Abstract

We set out to confirm the long-held, but untested, assumption that dietary salt affects proximal reabsorption through reciprocal effects on the renin-angiotensin system in a way that facilitates salt homeostasis. Wistar rats were fed standard or high-salt diets for 7 days and then subjected to renal micropuncture for determination of single-nephron GFR (SNGFR) and proximal reabsorption. The tubuloglomerular feedback (TGF) system was used as a tool to manipulate SNGFR in order to distinguish primary changes in net proximal reabsorption (Jprox) from changes due to glomerulotubular balance. The influence of Ang II over Jprox was determined by the sensitivity of Jprox to the AT1 receptor antagonist, losartan. Plasma, whole kidneys, and fluid from midproximal tubules were assayed for Ang II content by radioimmunoassay. In rats on the standard diet, losartan reduced Jprox by 25% and reduced the maximum range of the TGF response by 50%. The high-salt diet suppressed plasma and whole-kidney Ang II levels. But the high-salt diet failed to reduce the impact of losartan on Jprox or the TGF response and actually caused tubular fluid Ang II content to increase. The persistent effect of Ang II on Jprox prevented a major rise in late proximal flow rate in response to the high-salt diet. These observations challenge the traditional model and indicate that the role of proximal tubular Ang II in salt-replete rats is to stabilize nephron function rather than to contribute to salt homeostasis.

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Figure 1

Jprox as a function of SNGFR.

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Jprox as a function of SNGFR.
In order to make SNGFR an independent vari...
In order to make SNGFR an independent variable, Henle’s loop was perfused to alter the activity of tubuloglomerular feedback. Data points and error bars represent adjusted least-squares mean ± SEM. The vertical distance between the solid and dashed lines reflect primary differences in proximal reabsorption. Losartan reduced Jprox regardless of dietary salt (B and D). The high-salt diet increased SNGFR and Jprox (A), but had tubular Ang II been suppressed by the high-salt diet, the increase in Jprox would not have occurred (A and C). P < 0.05 for SNGFR >26 (A), SNGFR <26 (B), and all SNGFR (D).

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