Received February 5, 1985; accepted February 4, 1986. lease their granular content in a manner similar to that of nerve terminals. The aim of the present study was to determine whether platelet reactivity was altered in spontaneously hypertensive rats (SHR) and, if so, whether this alteration existed at the prehypertensive stage. In addition, we compared the functional response of platelets from hypertensive and control Wistar-Kyoto rats (WKY) to different external calcium concentrations to define the mechanism (or mechanisms) involved in the difference.Finally
Thrombin-induced calcium uptake and serotonin release were measured on platelets from spontaneously hypertensive rats (SHR) and normotensive control animals (WKY). Both 45Ca uptake and serotonin release induced by thrombin are enhanced in platelets from SHR in the presence of various Ca2+ concentrations. In the presence of [Ca2+] 10(-6)M a correlation exists between thrombin-induced calcium uptake and serotonin release; platelets from SHR and WKY do not differ in this respect, which demonstrates that the anomaly observed in platelets from SHR concerns an early reaction in the stimulation-response coupling. The inhibitory effect of magnesium on thrombin-induced serotonin release, less important in platelets from SHR than in control ones, seems to pass through two phenomena: an inhibition of calcium influx occurring at high concentrations and less effective on SHR platelets and a stimulation of calcium influx, probably corresponding to intracellular calcium sequestering, observed in the presence of low magnesium concentrations and enhanced in platelets from SHR. This study therefore evidence a relationship between the increases observed in both serotonin secretion and calcium influx on thrombin-stimulated SHR platelets and suggests cellular mechanisms involved in the inhibitory action of magnesium impaired in these SHR platelets.
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