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World J Nephrol. Nov 6, 2014; 3(4): 295-301
Published online Nov 6, 2014. doi: 10.5527/wjn.v3.i4.295
Regulatory roles of nitric oxide and angiotensin II on renal tubular transport
Shoko Horita, Motonobu Nakamura, Ayumi Shirai, Osamu Yamazaki, Nobuhiko Satoh, Masashi Suzuki, George Seki
Shoko Horita, Motonobu Nakamura, Ayumi Shirai, Osamu Yamazaki, Nobuhiko Satoh, Masashi Suzuki, George Seki, Department of Internal Medicine, The University of Tokyo, Tokyo 113-0033, Japan
Author contributions: All authors contributed to this paper.
Correspondence to: George Seki, MD, Department of Internal Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan. georgeseki-tky@umin.ac.jp
Telephone: +81-3-38155411 Fax: +81-3-58008806
Received: June 28, 2014
Revised: September 5, 2014
Accepted: October 1, 2014
Published online: November 6, 2014
Processing time: 132 Days and 3 Hours
Abstract

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 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/guanosine 3’,5’-cyclic monophosphate/extracellular signal-regulated 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.

Keywords: Angiotensin II; Nitric oxide; Proximal tubules; Thick ascending limb; Distal tubules; Na+ transport

Core tip: Angiotensin II (AngII) and nitric oxide (NO) play important roles in the regulation of renal tubular transport. AngII has a biphasic effect on renal proximal tubule (PTs) transport, and NO seems to inhibit the effect of AngII. In human PTs, however, AngII seems to have an NO-dependent monophasic stimulatory effect. We will discuss the recent findings in this field.