Changes in platelet function due to hypertension: comparison of experimental hypertension with spontaneous...

In washed platelets both from DOCA-salt and renal hypertensive rats, there was a marked decrease in thrombin-induced aggregation and secretion responses compared with those of respective controls. Concomitantly, the platelets showed attenuated malondialdehyde (MDA) formation and reduced serotonin contents, suggesting the presence of degranulated platelets in the circulation due to hypertension. In platelets from stroke-prone spontaneously hypertensive rats (SHRSP) at early hypertensive stages, thrombin-induced aggregation and secretion responses were similarly reduced. However, the platelet hypofunctions did not accompany reduced MDA formation and serotonin contents. Properties of platelets obtained from SHRSP at late hypertensive stages resembled those of platelets from experimentally hypertensive rats. These results suggest that the mechanisms of platelet hypofunction differ between experimental hypertension and spontaneous hypertension in their early stages. The hypo-aggregability observed in experimental hypertension appears to be secondary to the hypertension, whereas that seen in spontaneous hypertension seems to be a primary defect and not secondary to hypertension at early stages of hypertension.