Defective Ca2+ Functions in Protein (47-kDa) Phosphorylation and in the Coupling to Physiological Responses in Platelets from Stroke-Prone Spontaneously Hypertensive Rats
Although hypertension is assumed to be one of the important factors in thrombotic disease, inconsistent reports have been presented concerning changes in platelet function due to hypertension. Stroke-prone spontaneously hypertensive rats (SHRSP), a substrain of spontaneously hypertensive rats (SHR), which was established in 1974 (Okamotoet al., 1974), develops more severe hypertension spontaneously than SHR, and dies of massive cerebral hemorrhage or infarction between 100 and 300 days after birth. Changes in platelet functions were investigated using these strains of spontaneous hypertension which are considered to represent the closest model to human hypertension. In addition, platelets are a tissue in which pathophysiological changes are intimately related to those of blood vessels (Mustardet al., 1964). Both contain contractile proteins and Ca2+ plays important roles in both tissues (Weiss, 1975). Thus, the study of abnormalities in platelets from hypertensive animals may shed light on the etiology of hypertension as well as of diseases consequent to hypertension.
KeywordsPlatelet Function Protein Phosphorylation Serotonin Release Inositol Trisphosphate Phenacyl Bromide
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