Abnormal Ca²⁺ Handling and Increased Mg²⁺ Permeability in Platelets of Hypertensive Rats

Abstract

In order to test the hypothesis that intracellular Na⁺ accumulation and cellular Mg²⁺ deficiency may be involved in the abnormalities in Ca²⁺ handling and reactivity in spontaneously hypertensive rats (SHR) platelets, the metabolism of Na⁺, Ca²⁺ and Mg²⁺ was determined in fluorescent dye loaded platelets from 15 SHR and 15 Wistar-Kyoto rats (WKY) at 12 weeks of age. Mg²⁺ leak was estimated as the Mg²⁺ influx induced by an increase in extracellular [Mg²⁺] (from 1 to 5mmol/l) and Mg²⁺/Na⁺ exchange activity was estimated as the Mg²⁺ influx induced by a decrease in extracellular [Na⁺] (from 140 to 50mmol/l). Cellular metabolism of the fluorescent dye was similar in the two groups. Mean platelet [Ca²⁺]i was significantly increased under basal and thrombin (0.1U/ml)-stimulated conditions in SHR compared to WKY, both in the presence and absence of extracellular Ca²⁺. Mean Ca²⁺ discharge capacity was similar between the two groups. There was no difference in mean [Na⁺]i between the two groups. Basal [Mg²⁺]i was also increased in SHR platelets. Mg²⁺ leak was higher in SHR than in WKY, while Mg²⁺/Na⁺ exchange activity was similar in the two groups. There was no difference in serum Mg²⁺ concentration between SHR and WKY. These data suggest that abnormal Ca²⁺ handling is accompanied by elevation in [Mg²⁺]i via increased permeability of platelet cell membranes to Mg²⁺ in SHR without any alteration in [Na⁺]i, and do not support the Mg²⁺ deficiency hypothesis in genetically hypertensive rats. (Hypertens Res 2000; 23: 651-657)