title: Platelet thrombus formation in microvessels of young spontaneously hypertensive rats.
abstract: We have previously shown an increase in platelet-to-endothelial cell adhesion in microvessels of spontaneously hypertensive rats (SHR) during the established stage of hypertension (12 weeks). The objective of the current study was to determine if the platelet-to-endothelial cell interaction would be altered in the early developmental phase of hypertension. Male weanling (3 weeks old) SHRs (n=6) and age matched normotensive Wistar-Kyoto (WKY) rats (n=6) were used to study platelet thrombus formation. Intravascular fluorescein isothiocyanate tagged to bovine serum albumin was activated with 450-490 nm light to induce thrombus formation in microvessels. Plasma concentrations of von Willebrand factor (vWF), fibrinogen and fibronectin (FN) were measured in rats during both early (3 week) and established stages of hypertension development. 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 rats respectively. After thrombus appearance, however, overall time for vessel occlusion in arterioles (2590+/-90 sec) and venules (935+/-131 sec) of SHRs was not different compared to that in arterioles (2650+/-191 sec) and venules (1240+/-93 sec) of age matched WKY rats. The plasma concentration of FN was increased (p<0.05) in both the young (0.9+/-0.1 mg/ml) and mature (1.1+/-0.2 mg/ml) hypertensive rats (n=5) compared to that in young (0.6+/-0.03 mg/ml) and mature (0.5+/-0.1 mg/ml) WKY rats (n=5), while fibrinogen content (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 either age group of hypertensive animals. These results suggest that changes in platelet-to-endothelial cell interactions occur in the early phase of genetic hypertension development in rats, and appears to result from alteration of plasma concentration of adhesion proteins.
authors.affiliation: Center for Applied Microcirculatory Research, University of Louisville, KY 40292, USA.
authors.forename: D
authors.initials: D
authors.lastname: Lominadze
authors.forename: I G
authors.initials: IG
authors.lastname: Joshua
authors.forename: J L
authors.initials: JL
authors.lastname: Catalfamo
authors.forename: D A
authors.initials: DA
authors.lastname: Schuschke
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D001809:Blood Viscosity; D005340:Fibrinogen / Q000378:metabolism; D005353:Fibronectins / Q000378:metabolism; D006973:Hypertension / Q000150:complications / Q000503:physiopathology*; D008297:Male; D008833:Microcirculation / Q000502:physiology; D010973:Platelet Adhesiveness / Q000502:physiology*; D051381:Rats; D011918:Rats, Inbred SHR; D013927:Thrombosis / Q000150:complications / Q000503:physiopathology*; D014841:von Willebrand Factor / Q000378:metabolism
chemical_list: D005353:Fibronectins; D014841:von Willebrand Factor; D005340:Fibrinogen