ISSN:
1432-1041
Keywords:
Platelet aggregation, Ketanserin
;
sodium diet, pharma renin activity, platelet 5-HT2 receptor
Source:
Springer Online Journal Archives 1860-2000
Topics:
Chemistry and Pharmacology
,
Medicine
Notes:
Summary 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 · 1−1 in 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.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF02284963
