DIETARY SODIUM INTAKE DOES NOT ALTER RENAL POTASSIUM HANDLING AND BLOOD PRESSURE IN HEALTHY YOUNG MALES

Abstract

Objective: High salt intake and potassium deficiency are involved in the pathogenesis of hypertension and cardiovascular diseases. The effects of sodium intakes on renal handling of potassium are scarcely studied. The objective of this study is to assess the renal handling of potassium in condition of low, normal and high sodium intake. Design and method: In a cross-over study, we assessed the effect of sodium on renal potassium handling in 16 healthy males assigned to three 7-day periods on low (LSD, 3 g NaCl/d), normal (NSD, 6 g NaCl/d) and high (HSD, 15 g NaCl/d) sodium diet with constant potassium intake. Contributions of distal NaCl co-transporter and epithelial sodium channel in the collecting system on potassium and sodium handling were assessed at steady-state by acute response to 100 mg oral hydrochlorothiazide and with addition of 10 mg of amiloride to hydrochlorothiazide, respectively. Results: Diurnal blood pressure slightly increased from 119.30 ± 7.95 mmHg under LSD to 123.00 ± 7.50 mmHg, (P = 0.02) under HSD, while estimated glomerular filtration rate increased from 133.20 ± 34.68 ml/min under LSD to 187.00 ± 49.10 under HSD, (P = 0.005). Twenty-four hours potassium excretion remained stable on all sodium intakes (66.28 ± 19.12 mmol/24 h under LSD; 55.91 ± 21.17 mmol/24 h under NSD and 66.81 ± 20.72 under HSD, P = 0.9). The hydrochlorothiazide-induced natriuresis was the highest under HSD (30.22 ± 12.53 mmol/h), and the lowest under LSD (15.38 ± 8.94 mmol/h, P = 0.02). Hydrochlorothiazide increased kaliuresis and amiloride decreased kaliuresis similarly on all 3 diets. Conclusions: Neither spontaneous nor diuretic-induced potassium excretion were influenced by sodium intake in healthy male subjects. However, the respective contribution of the distal convoluted tubule and the collecting duct to renal sodium handling was dependent on dietary sodium intake.