High sodium intake increases platelet aggregation in normal females.

Platelet activation and aggregation appear to play an important part in the development of vascular disease. We studied the effect of varying sodium intake on total plasma serotonin and in vitro aggregation of blood platelets. A total of 12 normal female volunteers were studied after 5 days on a 10 or 200 mmol/day sodium diet. Aggregation studies were performed by incubating stirred platelet-rich plasma (PRP) with adenosine diphosphate (ADP) at final concentrations of 1 and 4 mumol/l; we also studied the effect of pre-incubating PRP with ketanserin or saralasin (1 mumol/l and 1 nmol/l final concentration, respectively). Salt-loading produced a significant increase in platelet aggregation induced by both 1 and 4 mumol/l ADP, and also a significant fall in PRP in serotonin concentration; since there was also a significant drop in the yield of platelets in PRP during salt-loading, the difference in serotonin concentration was not significant when expressed as pmol serotonin/10(8) platelets. There was a significant negative correlation between log serotonin levels (nmol/l) and % aggregation induced by 4 mumol/l ADP. Ketanserin decreased aggregation (induced by 4 mumol/l ADP) in PRP obtained during high salt intake; saralasin had no effect on aggregation, but did cause a decrease in light transmission. These results indicate that in normal females: (1) in vitro platelet aggregation is increased with high sodium intake, and this effect was reduced by addition of ketanserin; (2) PRP platelet count and total plasma serotonin levels are both significantly altered by changes in sodium status; (3) aggregation (%) is inversely proportional to log serotonin concentration (nmol/l).