Determinants of renal oxygen metabolism during low Na + diet: effect of angiotensin II AT 1 and aldosterone receptor blockade

Abstract

Reduced Na+ intake reduces the partial pressure of oxygen (PO2) 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 AT1 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 two weeks. Animals were anesthetized (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 the 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 impacted upon arterial pressure. Renal blood flow increased in both groups after candesartan as well as cortical oxygen tension, on low Na+ group. Fractional Na+ excretion was increased and oxygen consumption reduced on low Na+ group after CAP.

These results suggest that blockade of angiotensin II AT1 receptors have a major impact upon oxygen delivery during normal and low Na+, while aldosterone receptors mainly affect oxygen metabolism following two weeks of low Na+ diet.