Low Sodium Intake Causes Kidney Cortical Hypoxia and Proteinuria in Rats

Abstract

Reduced sodium intake induces activation of the renin‐angiotensin system to maintain sodium balance and arterial blood pressure. Renin‐angiotensin aldosterone system‐induced oxidative stress is a common pathway to intrarenal hypoxia, which could be detrimental if imposed on an already damaged kidney. We therefore investigated the effect of reduced sodium intake on kidney oxygen homeostasis and function in rats.Male Sprague Dawley rats were fed standard rat chow containing normal (0.25% sodium) or low sodium content (0.02%) for two weeks and kidney oxygen metabolism and function were studied thereafter. Acute blockade of angiotensin II AT1 receptors by candesartan (1 mg kg−1) was used to estimate the degree of renin‐angiotensin system activation in combination with measurements of intrarenal tissue angiotensin II levels.Dietary sodium restriction increased intrarenal angiotensin II tissue levels without altered arterial blood pressure. Concomitantly, a pronounced increase in kidney oxygen consumption was observed along with reduced tubular electrolyte transport efficiency and abolished cortico‐medullary oxygen gradient. Urinary protein excretion increased although renal blood flow and glomerular filtration rate were preserved.In conclusion, reduced sodium intake causing renin‐angiotensin‐aldosterone system activation significantly increases kidney oxygen consumption resulting in cortical tissue hypoxia and proteinuria. This is possibly an undesired effect, especially during pre‐existing kidney disease.Support or Funding InformationSwedish Research Council, Swedish Diabetes Foundation, Swedish Heart‐Lung Foundation and Family Ernfors Fund.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.