Fatty acid binding protein was purified from renal medulla, and its binding activity and fatty acid composition were determined in spontaneously hypertensive stroke-prone rats. Wistar-Kyoto rats were used as controls. Fatty acid binding activity was higher in 5-week-old prehypertensive spontaneously hypertensive stroke-prone rats (0.155 +/- 0.006 mol palmitic acid/mol protein) as compared with control values in Wistar-Kyoto rats (0.030 +/- 0.001). However, in 40-week-old rats, the activity was decreased only in spontaneously hypertensive stroke-prone rats with established hypertension (0.035 +/- 0.002), and it did not decrease in Wistar-Kyoto rats (0.028 +/- 0.003). Fatty acid compositions were similar among 5 and 40-week-old control rats and 5-week-old hypertensive rats (palmitic acid 24%, stearic acid 14%, oleic acid 30%, linoleic acid 29%, arachidonic acid 3%), although the total amount of bound long-chain fatty acids was decreased in 5-week-old hypertensive rats, explaining the high fatty acid binding activity in this preparation. Fatty acid binding protein from 40-week-old hypertensive rats had an elevated proportion of endogenous arachidonic acid, with other fatty acids being relatively reduced (palmitic acid 8%, stearic acid 2%, oleic acid 4%, linoleic acid 10%, arachidonic acid 76%), indicating increased arachidonic acid transport in the cytosol. These results show that genetically hypertensive rats had an alteration in fatty acid transport mediated by fatty acid binding protein; this alteration may be involved in the pathogenesis of hypertension.