PLATELET THROMBUS FORMATION IN MICROVESSELS OF YOUNG SPONTANEOUSLY HYPERTENSIVE RATS

We have previously shown an increase in platelet-to-endothelial cell a dhesion in microvessels of spontaneously hypertensive rats (SHR) durin g the established stage of hypertension (12 weeks). The objective of t he current study was to determine if the platelet-to-endothelial cell interaction would be altered in the early developmental phase of hyper tension. Male weanling (3 weeks old) SHRs (n=6) and age matched normot ensive Wistar-Kyoto (WKY) rats (n=6) were used to study platelet throm bus formation. Intravascular fluorescein isothiocyanate tagged to bovi ne serum albumin was activated with 450-490 nm light to induce thrombu s formation in microvessels. Plasma concentrations of von Willebrand f actor (vWF), fibrinogen and fibronectin (FN) were measured in mts duri ng both early (3 week) and established stages of hypertension developm ent. Thrombus initiation time in both arterioles (847 +/- 85 sec) and venules (222 +/- 40 sec) of young SHRs was significantly shorter (p<0. 05) than in arterioles (1270 +/- 88 sec) and venules (630 +/- 72 sec) of age matched WKY mts respectively. After thrombus appearance, howeve r, overall time for vessel occlusion in arterioles (2590 +/- 90 sec) a nd venules (935 +/- 131 sec) of SHRs was not different compared to tha t in arterioles (2650 +/- 191 sec) and venules (1240 +/- 93 sec) of ag e matched WKY rats. The plasma concentration of FN was increased (p<0. 05) in bath the young (0.9 +/- 0.1 mg/ml) and mature (1.1 +/- 0.2 mg/m l) hypertensive mts (n=5) compared to that in young (0.6 +/- 0.03 mg/m l) and mature (0.5 +/- 0.1 mg/ml) WKY rats (n=5), while fibrinogen con tent (3.6 +/- 0.3 mg/ml) was elevated (p<0.05) only in mature SHRs (n= 5) compared to that (2.7 +/- 0.02 mg/ml) in age matched WKY rats (n=5) . The plasma concentration of vWF was similar to that of controls in e ither age group of: hypertensive animals. These results suggest that c hanges in platelet-to-endothelial cell interactions occur in the early phase of genetic hypertension development in rats, and appears to res ult from alteration of plasma concentration of adhesion proteins.