PP.16.18

Abstract

Objective: In rats, high sodium intake augments adenosine-induced vasodilation (Liclican EL et al. 2005 and Dobrowolski L et al. 2007). This study tests the hypothesis that the acute blood pressure response to caffeinated coffee (adenosine receptor antagonist) is augmented by high sodium intake in humans. Design and method: 13 healthy volunteers (8 male) used low (LS; 6 gram/24 hours) and high (HS; 12 gram/24 hours) salt diet in random order, each for 5 days with 4 day wash-out. At the end of each diet and after 24 hours of caffeine abstinence, subjects drank 350 ml of caffeinated coffee. Primary endpoint was the blood pressure response (Dinamap 1846 SX; Critikon, Portanje Electronica BV) to coffee. Results: Maintenance to the diet was confirmed by urinary sodium excretion (5 ± 2 (SD) versus 12 ± 4 g NaCl/24 hours, p < 0,0001). Plasma caffeine concentration significantly increased from 0.2 ± 0.2 (SD) to 6.6 ± 1.8 μg/ml (p > 0.3 for comparison between 2 days, paired t-test). Table: Course in blood pressure (mean ± SEM (mmHg)*p < 0.05 versus low salt; #p < 0.01 for increase over time. The interaction between high and low sodium diet and caffeine intake on SBP, DBP (p > 0,3) and MAP (p > 0,05) was not statistically significant (ANOVA for repeated measures). SBP: Systolic Blood Pressure; DBP: Diastolic Blood Pressure; MAP: Mean Arterial Blood Pressure. Conclusions: High sodium intake does not augment the acute blood pressure response to coffee. This observation does not support a mitigating role of adenosine on the salt-associated increase in blood pressure in humans.