Determinants of renal oxygen metabolism during low Na⁺ diet: effect of angiotensin II AT₁ and aldosterone receptor blockade

Abstract

Reducing Na + intake reduces the partial pressure of oxygen in the renal cortex and activates the renin-angiotensin-aldosterone system. r In the absence of high blood pressure, these consequences of dietary Na + reduction may be detrimental for the kidney. r In a normotensive animal experimental model, reducing Na + intake for 2 weeks increased renal oxygen consumption, which was normalized by mineralocorticoid receptor blockade. Furthermore, blockade of the angiotensin II AT 1 receptor restored cortical partial pressure of oxygen by improving oxygen delivery. r This shows that increased activity of the renin-angiotensin-aldosterone system contributes to increased oxygen metabolism in the kidney after 2 weeks of a low Na + diet. r The results provide insights into dietary Na + restriction in the absence of high blood pressure, and its consequences for the kidney.

Renal blood flow and oxygenation

“…Moreover, Ang II stimulates Na + transporter abundance and activity, particularly in the distal nephron [ 48 ] where T Na /Q O2 is lower, which also raises O 2 consumption. Palm and colleagues recently demonstrated that activation of the renin-angiotensin-aldosterone system by a low Na + diet increased Q O2 and lowered cortical pO 2 but raised medullary pO 2 [ 49 ]; a similar low-salt diet-induced reversal of pO 2 gradients was previously observed [ 50 ]. Of note, AT1 receptor blockade restored pO 2 without reducing Q O2 , confirming the major impact of Ang II on renal O 2 delivery [ 49 ].…”

Low‐salt diet and renal safety: taken with a pinch of salt

“…The study by Patinha et al . (2020) published in this issue of The Journal of Physiology addresses RAAS‐mediated adaptive changes to a 10‐fold salt restriction, involving the renal microcirculation, tubular sodium handling and oxygen expenditure, providing novel perspectives on the control of renal oxygenation.…”

“…Patinha et al . (2020) report that extreme salt depletion in normotensive rats reduces cortical oxygenation and increases sodium retention, oxygen consumption and extraction with decreased transport work efficacy. Assessing the role of activated RAAS in these changes, they found that candesartan infused into the renal artery did not affect blood pressure and GFR but restored cortical oxygenation, principally by increasing renal blood flow and oxygen delivery.…”

“…Furthermore, as now also confirmed by Patinha et al . 2020, salt restriction led to an inverted profile of renal parenchymal oxygenation, with reduced cortical and increased medullary oxygenation (Stillman et al . 1994).…”