Abstract
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 2weeks increased renal oxygen consumption, which was normalized by mineralocorticoid receptor blockade. Furthermore, blockade of the angiotensin II AT1 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 2weeks 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. 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 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 2weeks. The animals were anaesthetized (thiobutabarbital 120mgkg-1 ) and surgically prepared for kidney oxygen metabolism and function studies before and after acute intrarenal arterial infusion of candesartan (4.2μgkg-1 ) or intravenous infusion of CAP (20mgkg-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 AT1 receptors has a major impact upon oxygen delivery during normal and low Na+ conditions, while aldosterone receptors mainly affect oxygen metabolism following 2weeks of a low Na+ diet.
Highlights
IntroductionRenal oxygen content is determined by delivery and demand. Renal autoregulation maintains renal blood flow (RBF) within a wide range of perfusion pressures to maintain a stable glomerular filtration rate (GFR)
As in other organs, renal oxygen content is determined by delivery and demand
Increased renin-angiotensin-aldosterone system (RAAS) activity in the low Na+ group was confirmed by increased intrarenal tissue concentrations of angiotensin II (Table 2)
Summary
Renal oxygen content is determined by delivery and demand. Renal autoregulation maintains renal blood flow (RBF) within a wide range of perfusion pressures to maintain a stable glomerular filtration rate (GFR). We and others have shown that prolonged increased oxygen consumption (Q O2), low PO2 along the renal parenchyma and consequent renal hypoxia are associated with long-term renal impairment (Welch et al 2001; Manotham et al 2004; Matsumoto et al 2004; Palm et al 2004; Friederich-Persson et al 2013; Ow et al 2014; Franzen et al 2016; Emans et al 2018). The major determinant of renal oxygen metabolism is Na+ transport (Brezis et al 1994a). Increased kidney Q O2 can result from increased tubular Na+ reabsorption to compensate for either glomerular hyperfiltration (Korner et al 1994) or oxidative stress-induced reduction of electrolyte transport efficiency (Palm et al 2003; Welch et al 2003, 2005). Increasing Na+ reabsorption in downstream segments of the nephron may lead increased total kidney Q O2
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