This study was designed to determine roles of renal sympathetic nerve activity (RNA) and adrenal catecholamines in the changes of renal vascular resistance during prolonged hemorrhagic shock in anesthetized dogs. In animals with intact baroreceptors, hemorrhagic hypotension (40 mm Hg) caused RNA to increase significantly within 1 min after bleeding, followed by a return to baseline within 10 min. Thereafter, a secondary increase in RNA occurred that was followed by a gradual decline towards the baseline level. The renal perfusion pressure (RPP) showed a progressive and significant increase until the end of the experiment. The initial increase in RNA was abolished by complete denervation of the systemic baroreceptors. The initial increase in RPP, which was observed within 10 min after bleeding in animals with intact baroreceptors, was attenuated by the denervation. In animals with bilateral adrenalectomy, RPP still showed an initial increase, but the progressive increase throughout the entire experimental period did not occur. In animals with baroreceptor denervation and bilateral adrenalectomy, RPP did not show any significant changes during the experiment. These results indicate that the initial renal vasoconstrictive response to hemorrhage is regulated by a reflex sympathetic mechanism. In contrast, a late renal vasoconstriction during hemorrhagic hypotension is predominantly evoked by humoral substances such as adrenal catecholamines.