Angiotensin II (AngII) exerts powerful effects on the renal microcirculation to influence a variety of functions. This review summarizes some of the major findings over the past 10 years as they elucidate the multiple roles that AngII plays in the regulation of whole kidney blood flow, perfusion of cortical and medullary regions, and renal autoregulation. Topics of discussion include localization of AngII receptor types and subtypes in the renal vasculature, action of AngII on vascular smooth muscle cells of the afferent and efferent arterioles, and intracellular signaling pathways. Within the microvasculature, AngII causes potent constriction in both the afferent and efferent arterioles, with responses modulated by paracrine and autocrine factors of endothelial and macula densa origins. With regard to renal autoregulatory mechanisms consisting of the myogenic response and the tubuloglomerular feedback mechanism, the myogenic response appears to operate independent of the renin-angiotensin system. On the other hand, tubuloglomerular feedback activity is often directly proportional to concentrations of AngII, especially in high renin states. Of the two types defined to date, the AT1 is the predominant receptor in the adult rat kidney mediating the vascular effects of AngII. AT2 receptor is highly expressed in the fetal kidney and is important for renal development, but is very weakly expressed in adult animals. Nevertheless, AT2 receptors may mediate vasodilation under certain conditions. The signaling transduction pathways for AT1 receptors include Gq/11-protein and protein kinase C activation. AngII causes constriction of the afferent arteriole primarily by stimulation of calcium entry via voltage-sensitive, L-type channels, whereas AngII effects on the efferent arteriole are due to calcium release from intracellular stores and calcium entry through voltage-independent calcium entry channels. Future experiments should contribute to a more in-depth understanding of the modulation of AngII effects by other vasoactive agents and interactions between different second-messenger signaling pathways in health and disease.