1. Hypofunction of stroke-prone spontaneously hypertensive rat (SHRSP) platelets at developmental ages of hypertension is due to the defective protein (p47) phosphorylation which is mediated by protein kinase C. This study was undertaken to examine the genetic association of platelet functions and vascular reactivity with hypertension using male WKY, SHRSP, F1 and backcross generations at 16-18 weeks of age. 2. The distribution of blood pressure was continuous in each generation. 3. Contraction of mesenteric vascular bed with norepinephrine was positively correlated with blood pressure in the five generations (r = 0.77, n = 128). 4. Thrombin-induced platelet aggregation was inversely correlated with blood pressure (r = -0.87, n = 127). 5. The distribution of platelet aggregation and contraction was continuous in each generation, and backcross generations were not likely to have 1:1 segregation. 6. These results suggest the possibility that platelet hypoaggregability and peripheral vascular resistance are due to the pleiotropic effect of hypertensive genes, or that genes controlling these three characters are closely linked each other.