Why the study?
Does hypertension and its treatment with prazosin affect arterial thrombus formation and platelet aggregation in spontaneously hypertensive rats?
Does hypertension and its treatment with prazosin affect arterial thrombus formation and platelet aggregation in spontaneously hypertensive rats?
High blood pressure directly interferes with thrombus establishment, and platelet hypoaggregability partly contributes to prolonged thrombogenesis in spontaneously hypertensive rats.
Hypertension may prolong thrombogenesis in rat models via platelet effects; leaves open relevance to human arterial thrombosis and antihypertensive therapy.
The present study was conducted to investigate the effect of hypertension on the formation of arterial thrombus in the rat femoral artery. The time required to establish the thrombus following endothelial injury in spontaneously hypertensive rats (SHR) was extremely prolonged. Pretreatment with prazosin which lowered the blood pressure near the level in normotensive Wistar Kyoto (WKY) rats, significantly shortened the thrombogenesis time, but it was still longer than that in WKY rats. Platelet aggregation in response to collagen with washed platelets and whole blood was reduced in SHR with and without hypotensive treatment, in comparison with that in WKY rats. Prazosin did not affect the platelet aggregability. Therefore, the decreased platelet aggregation was considered to be responsible for the delayed thrombus formation in hypotensively treated SHR. These results suggested that high blood pressure, mainly, interferes with the establishment of thrombus directly. Hypoaggregability of platelets is likely to be partly involved in the prolongation of thrombogenesis in SHR.
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Takiguchi et al. (1993) studied this question.
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