Normal thrombin binding leads to greater fibrinogen binding and increased platelet aggregation in spontaneously hypertensive rats

In Vivo Platelet Thrombus Formation in Microvessels of Spontaneously Hypertensive Rats

“…These results suggest that the alterations of the platelet aggregation are independent from wall shear rate changes. Even though in vitro platelet aggregation has been reported to be increased during hypertension, 7 the decreased in vivo platelet aggregation in the SHR group in the present study corresponds with other in vivo as well as in vitro work, 21 which points to a greater effect of the first stage of thrombogenesis, ie, platelet adhesion to vessel wall, during genetically induced hypertension.…”

“…Although increased number of platelets is not a mechanism associated with increased thrombogenesis in the hypertensive phenotype, 32 it may be caused by changes in platelet function. 7 The present results demonstrate that the normal hemostatic function of platelets is changed by altered blood rheological and endothelial cell properties induced by chronically elevated mean arterial pressure. In conclusion, we suggest that the increased thrombus formation during the development of genetic hypertension is mainly the result of an altered platelet-to-endothelial cell interaction.…”

“…An increased concentration of adhesive protein vWF 23 and increased fibrinogen binding 7 in SHRs is another plausible mechanism for hypertension-induced enhanced thrombogenesis in the response to acute focal injury. Although vWF is thought to have a greater effect at higher wall shear rates (arterioles), 24,25 our previous results, 26 in agreement with Ross et al, 25 have shown vWF's importance at lower wall shear rates as well.…”

“…These include increased whole blood viscosity at low (Ͻ208 sec Ϫ1 ) shear rates, 1,2 increased plasma viscosity, 1,2 enhanced plasma proteins vWF, 3 and particularly fibrinogen 4 concentrations, which are the major determinants of plasma viscosity. Hematocrit 2 and erythrocyte 2,5,6 and platelet 7,8 aggregation indices are also increased during hypertension.…”

“…Similar to the clinical studies with humans, there are no reported in vivo studies involving the direct observation of platelet thrombus formation in the resistance vessels of spontaneously hypertensive (SHR) and Wistar Kyoto (WKY) rats. Because erythrocyte and platelet aggregation indices are increased in hypertension 2,[5][6][7][8] and production of the vasodilator/antiaggregatory agent nitric oxide (NO) is depressed in the SHR model, 12 we hypothesized that thrombogenesis would be increased in SHR in vivo.…”