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

Key points Reducing Na + intake reduces the partial pressure of oxygen in the renal cortex and activates the renin‐angiotensin‐aldosterone system. In the absence of high blood pressure, these consequences of dietary Na + reduction may be detrimental for the kidney. 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. 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. The results provide insights into dietary Na + restriction in the absence of high blood pressure, and its consequences for the kidney. Abstract Reduced Na + intake reduces the (partial pressure of oxygen) in the renal cortex. Upon reduced Na + intake, reabsorption along the nephron is adjusted with activation of the renin‐angiotensin‐aldosterone system (RAAS). Thus, we studied the effect of reduced Na + intake on renal oxygen homeostasis and function in rats, and the impact of intrarenal angiotensin II AT 1 receptor blockade using candesartan and mineralocorticoid receptor blockade using canrenoic acid potassium salt (CAP). Male Sprague‐Dawley rats were fed standard rat chow containing normal (0.25%) and low (0.025%) Na + for 2 weeks. The animals were anaesthetized (thiobutabarbital 120 mg kg −1 ) and surgically prepared for kidney oxygen metabolism and function studies before and after acute intrarenal arterial infusion of candesartan (4.2 μg kg −1 ) or intravenous infusion of CAP (20 mg kg −1 ). Baseline mean arterial pressure and renal blood flow were similar in both dietary groups. Fractional Na + excretion and cortical oxygen tension were lower and renal oxygen consumption was higher in low Na + groups. Neither candesartan nor CAP affected arterial pressure. Renal blood flow and cortical oxygen tension increased in both groups after candesartan in the low Na + group. Fractional Na + excretion was increased and oxygen consumption reduced in the low Na + group after CAP. These results suggest that blockade of angiotensin II AT 1 receptors has a major impact upon oxygen delivery during normal and low Na + conditions, while aldosterone receptors mainly affect oxygen metabolism following 2 weeks of a low Na + diet.