As indicated by changes in microsphere distribution in the rat, acute bilateral carotid artery occlusion (CAO) was found to cause a small but significant increase in outer cortical flow fraction. When renal perfusion pressure was kept constant, no redistribution occurred upon CAO. In denervated kidneys the redistribution induced by CAO did not differ from that observed in contralateral control kidneys. Animals pretreated with prostaglandin inhibitors showed a significant redistribution in the ‘unprotected’ right kidney and a minor increase in outer cortical flow fraction in the normotensive kidney. It is concluded that: (1) the increase in outer cortical flow fraction induced by CAO in the rat is due to an increase in perfusion pressure, and (2) that this redistribution is independent of sympathetic vasoconstrictor stimuli, catecholamines and prostagland