Calcium Supplementation Attenuates an Enhanced Platelet Function in Salt-Loaded Mildly Hypertensive Patients

Abstract

Abstract We designed this study to evaluate the effect of low versus high calcium intake on platelet function in salt-loaded patients with mild hypertension. After a 7-day period of dietary salt restriction, 19 patients were placed on a high salt (300 mmol/d), low calcium (6.25 mmol/d) diet for 7 days; 10 of these patients were given 54 mmol/d of supplementary calcium, and 9 patients were given placebo. At the end of the low and high salt regimens, we evaluated changes in blood pressure, platelet aggregation, and the platelet release reaction measured as plasma β-thromboglobulin and platelet factor 4 levels. With high salt intake, significant increases in mean blood pressure ( P <.02), red blood cell sodium ( P <.01), and platelet aggregation induced by 3 μmol/L ADP ( P <.01) and by 3.0 mg/L epinephrine ( P <.05) were observed in the placebo-treated patients but not in the calcium-supplemented ones. Compared with the placebo-treated patients, calcium-supplemented patients had a smaller weight gain ( P <.05) but excreted more sodium and calcium ( P <.01) at the end of the high salt regimen. Calcium supplementation resulted in decreases in β-thromboglobulin ( P <.05), platelet factor 4 ( P <.01), and plasma and urinary excretions of norepinephrine ( P <.02) during the high salt, low calcium regimen. The decrease in plasma norepinephrine correlated positively with the decreases in β-thromboglobulin ( r =.72, P <.02) and platelet factor 4 ( r =.85, P <.01). These results indicate that calcium supplementation prevents salt-induced high blood pressure and platelet hyperaggregability, with a suppression of the platelet release reaction. The beneficial effects of oral calcium for reducing thrombotic cardiovascular risk during high salt intake may partly be attributed to an attenuation of intracellular sodium retention and a decrease in sympathetic nervous activity.