Abstract
Salt-loading to SHRSP from 9 weeks of age caused a gradual decrease in both platelet count (PC) and platelet aggregability (PA) with the concomitant gradual increase of blood pressure (BP). The abnormal excretion of urinary protein (UP) began at 2-4 weeks after the beginning of salt-loading, when PC and PA declined to 6-7×105/mm3 and to 20%, respectively, and when the BP reached to 230-240mmHg. In these changes, inverse correlations were found between both PC and BP, and PA and BP.
Platelets from normal Wistar-Kyoto rats (WKY) aggregated normally in the presence of PPP from the SHRSP with a lowered aggregability. While, the decreased aggregability of SHRSP platelets was not repaired at all by incubation of the platelets with PPP from normal WKY. The release of radioactivity from 14C-serotonin-labeled platelets of the SHRSP with a lowered aggregability was also drastically decreased. These results indicate that the poor PA of SHRSP observed prior to the excretion of UP is derived from some dysfunction of the platelets.
From these observations, it is suggested that studies of platelets are useful for predicting the development of stroke before its clinical recognition.
