Our previous study demonstrated that high potassium (K) diets reduce stroke mortality in stroke-prone spontaneously hypertensive rats (SHRsp) even when the blood pressure is not lowered. On the other hand, macrophage infiltration into the vascular wall is known to play an important role in the development of arterial lesions. In this study, in vivo and in vitro experiments were performed to examine the effect of high K diets on macrophage adherence to the vascular wall in SHRsp rats. In the in vivo study, <sup>51</sup>Cr-labelled macrophages, collected from the peritoneal cavity, were injected intravenously to SHRsp rats fed 6% high NaCl diets containing either normal 0.5% K or high 2.1 % K, and, 45 min later, the rats were perfused with buffered saline to remove blood. Radioactivity from macrophages in the aorta was 40% lower in the high K SHRsp than in the normal K SHRsp (p < 0.002), and the brain of high K SHRsp also showed a 52% lower macrophage radioactivity than that of normal K SHRsp (p < 0.007). Although the mean blood pressure was slightly lower in the high K diet group than in the normal K diet group (167 vs. 184 mm Hg), these differences remained still prominent even when we compared groups with matching blood pressures; –33% for the aorta (p < 0.02) and –55% for the brain (p < 0.02). In the in vitro study, the aortas of SHRsp rats similarly fed on normal or high K diet were excised and mounted in a perfusion chamber. They were perfused with labelled macrophages at normotensive or hypertensive pressure. In normal K SHRsp, macrophage radioactivity remained in the washed aorta was 158% higher in high perfusion pressure group than in normal pressure (p < 0.002). However, they did not significantly differ between two perfusion pressures in high K SHRsp. These results indicate that high K diets reduce endothelial injuries which allow adherence and infiltration of macrophages into the vascular wall of hypertensive animals, and thereby contribute to the reduction of vascular lesions and stroke mortality.