Renal tubules regulate blood pressure and humoral homeostasis.Mediators that play a significant role in regulating the transport of solutes and water include angiotensin Ⅱ(AngⅡ) and nitric oxide(NO).AngⅡ can significantly raise blood pressure via effects on the heart,vasculature,and renal tubules.AngⅡ generally stimulates sodium reabsorption by triggering sodium and fluid retention in almost all segments of renal tubules.Stimulation of renal proximal tubule(PT) transport is thought to be essential for AngⅡ-mediated hypertension.However,AngⅡ has a biphasic effect on in vitro PT transport in mice,rats,and rabbits:stimulation at low concentrations and inhibition at high concentrations.On the other hand,NO is generally thought to inhibit renal tubular transport.In PTs,NO seems to be involved in the inhibitory effect of AngⅡ.A recent study reports a surprising finding:AngⅡ has a monophasic stimulatory effect on human PT transport.Detailed analysis of signalling mechanisms indicates that in contrast to other species,the human NO/guanosine3’,5’-cyclic monophosphate/extracellular signal-regulated kinase pathway seems to mediate this effect of AngⅡ on PT transport.In this review we will discuss recent progress in understanding the effects of AngⅡ and NO on renal tubular transport. Renal tubules regulate blood pressure and humoral homeostasis. Mediators that play a significant role in regulating the transport of solutes and water include angiotensin II (Ang II) and nitric oxide (NO). AngII can significantly raise blood pressure via effects on the heart, vasculature, and renal tubules. AngⅡ generally stimulates sodium reabsorption by triggering sodium and fluid retention in almost all segments of renal tubules. Promotion of renal proximal tubule (PT) transport is thought to be essential for Ang II-mediated hypertension. However, Ang II has a biphasic effect on in vitro PT transport in mice, rats, and rabbits: stimulation at low concentrations and inhibition at high concentrations. On the other hand, NO is generally thought to inhibit renal tubular transport. In PTs, NO seems to be involved in the inhibitory effect of Ang II. A recent study reports a surprising finding: Ang II has a monophasic stimulatory effect on human PT transport. Detailed analysis of signaling mechanisms in dicates that in contrast to other species, the human NO / guanosine 3 ’, 5’-cyclic monophosphate / extracellular signal-regulated kinase pathway seems to mediate this effect of AngⅡ on PT transport. this review we will discuss recent progress in understanding the effects of Ang II and NO on renal tubular transport.