Regulatory roles of nitric oxide and angiotensin Ⅱ 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(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 （AngⅡ） and nitric oxide （NO）. AngⅡcan signifcantly raise blood pressure via effects on the heart, vasculature, and renal tubules. AngⅡ generally stimulates sodium reabsorption by triggering sodium and fuid retention in almost all segments of renal tu-bules. Stimulation of renal proximal tubule （PT） trans-port is thought to be essential for AngⅡ-mediated hy-pertension. However, AngⅡ has a biphasic effect on in vitro PT transport in mice, rats, and rabbits： stimulation at low concentrations and inhibition at high concentra-tions. 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 fnding： AngⅡ has a mono-phasic stimulatory effect on human PT transport. De-tailed analysis of signalling mechanisms indicates that in contrast to other species, the human NO/guanosine 3’,5’-cyclic monophosphate/extracellular signal-regulat-ed kinase pathway seems to mediate this effect of Ang Ⅱ on PT transport. In this review we will discuss recent progress in understanding the effects of AngⅡ and NO on renal tubular transport.