We have investigated the effect of varying sodium intake on the renin-angiotensin system, ADP-induced patelet aggregationin vitro, and blood 5-HT concentrations in 9 male volunteers.
Systolic blood pressure was slightly reduced during a low sodium diet, whereas the diastolic pressure remained unchanged. Plasma renin activity and aldosterone concentration both fell significantly when sodium intake was increased; plasma angiotensin lI concentraion also fell, but not significantly.
There was a significant fall in haematocrit after an increased sodium intake, but there was no change in the whole-blood platelet count after correcting for this. There were no significant changes in either total (i. e. PRP) or platelet 5-HT concentrations.
The extent of platelet aggregation induced by 5 and 20 μmol · 1−1 of ADP increased significantly when dietary sodium intake was increased. When compared with low or normal sodium intakes, lower concentrations of ADP were required to produce 50% of maximum aggregation after a high sodium intake. The 5-HT2, receptor antagonist ketanserin (1 μmol · 1−1in vitro) reduced the extent of aggregation induced by 5 μmol · 1−1 ADP after the volunteers had taken a high sodium diet, whereas the angiotensin 11 receptor anatgonist saralasin (1 nmol-1−1) increased the rate of aggregation after the low sodium diet.
Thus, during a high sodium intake, human platelets become more sensitive to the aggregating agent ADP It is possible that this effect is mediatedvia platelet 5-HT2 receptors, since ketanserin abolished the increase in salt-induced aggregation seen with 5 μmol · 1−1 ADP.