Sodium-Sensitive Elevation in Blood Pressure is ENaC Independent in Diet-Induced Obesity and Insulin Resistance.

Sodium-Sensitive Elevation in Blood Pressure is ENaC Independent in Diet-Induced Obesity and Insulin Resistance. Am J Physiol Renal Physiol. 2016 Feb 3;:ajprenal.00265.2015 Authors: Nizar JM, Dong W, McClellan RB, Labarca M, Zhou Y, Wong J, Goens DG, Zhao M, Velarde N, Bernstein D, Pellizzon M, Satlin LM, Bhalla V Abstract The majority of patients with obesity, insulin resistance, and the metabolic syndrome have hypertension, but the mechanisms of hypertension are poorly understood. In these patients, impaired sodium excretion is critical for the genesis of sodium-sensitive hypertension, and prior studies have proposed a role for the epithelial sodium channel (ENaC) in this syndrome. We characterized high fat-fed mice as a model in which to study the contribution of ENaC-mediated sodium reabsorption in obesity and insulin resistance. High fat-fed mice demonstrated impaired sodium excretion and elevated blood pressure that was significantly higher on a high sodium diet compared to low fat-fed controls. However, high fat-fed mice had no increase in ENaC activity as measured by sodium transport across microperfused cortical collecting ducts, electrolyte excretion, or blood pressure. In addition, we found no difference in endogenous urinary aldosterone excretion between groups on a normal or high sodium diet. High fat-fed mice provide a model of metabolic syndrome, recapitulating obesity, insulin resistance, impaired natriuresis, and a s...
Source: Am J Physiol Renal P... - Category: Urology & Nephrology Authors: Tags: Am J Physiol Renal Physiol Source Type: research