The anticoagulant role of the vascular wall suggests that there are connections between coagulation and the phenotype of vascular smooth muscle cells (VSMCs). Our objective was to determine whether hypertension confers a hypercoagulable state. We used the model of spontaneously hypertensive rats (SHR) compared with Wistar rats. The reactivity of the coagulation system was studied in vitro by monitoring the kinetics of thrombin generation (Thrombography) in two experimental conditions: (i) the plasma in the presence or absence of thoracic aortic rings and (ii) on the surface of cultured VSMCs from aortas of rats in the presence of platelet-poor plasma of Wistar rats.
At baseline, plasma from SHR has a rate of thrombin generation significantly lower (p < 0.05) than the control. The addition of aortic rings of SHR to a pool of plasma from Wistar rats results in a significant increase in thrombin generation compared to the addition of rings of Wistar rats (699 ± 23 vs. 637 ± 8 nM.min, p < 0.05) to the same pool control. At the surface of cultured VSMC from SHR, thrombin generation was significantly higher than at the surface of VSMCs from Wistar rats (636 ± 10 versus 490 ± 12 nM.min, p < 0.05).
These results show that the wall of the SHR is more thrombotic than the vessel wall of Wistar rat. This phenotype is partly due to the ability of VSMCs to serve as a cellular support for the generation of thrombin. These results, obtained in vitro without hemodynamic stresses suggest a specific structural effect of the arterial wall producing an increased stiffness.