The purpose of my study was to assess a North American, Japanese-style diet commercially available from Zeigler Brothers (Gardners, Pennsylvania) with respect to the initiation of stroke development in 34 stroke-prone spontaneously hypertensive rats (spSHR) and in 14 strokeresistant spontaneously hypertensive rats (srSHR). Nineteen spSHR fed the diet containing 4% NaCl and 0.75% K + (low-K + diet) from weaning had an accelerated rate of stroke development (mean±SEM age at death 15.3±0.5 weeks). The same diet containing 2.11% K + (high-K + diet) increased the mean lifespan of 15 spSHR by 39% but did not prevent stroke. The locations of hemorrhagic lesions were similar in the groups of spSHR fed high-and low-K + diets, being nearly equally divided between the territories of the anterior, posterior, and middle cerebral arteries. The 14 srSHR fed the Iow-K + diet exhibited 50% mortality at 66 weeks of age. However, in the srSHR fed the Iow-K + diet, death did not result from hemorrhagic stroke. The differing incidence of stroke between the spSHR fed high-and low-K + diets and between spSHR and srSHR fed the low-K + diet could not be explained on the basis of differing blood pressures. Compared with spSHR fed the low-K + diet, both srSHR fed the low-K + diet and spSHR fed the high-K* diet exhibited higher drinking and urine excretion rates and elevated plasma K + levels. My study indicates the availability of a commercial North American diet that produces a predictable high incidence of stroke within a compressed time period in spSHR but not in srSHR. This diet would be useful in studies attempting to determine the events preceding and leading to the development of stroke and in determining the genetic factors responsible for stroke resistance.