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Copyright © 2014 Motonobu Nakamura et al. Motonobu Nakamura et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Sodium-coupled bicarbonate absorption from renal proximal tubules (PTs) plays a pivotal role in the maintenance of systemic acid/base balance. Indeed, mutations in the Na+-HC[superscript][subscript]O3[/subscript] -[/superscript] cotransporter NBCe1, which mediates a majority of bicarbonate exit from PTs, cause severe proximal renal tubular acidosis associated with ocular and other extrarenal abnormalities. Sodium transport in PTs also plays an important role in the regulation of blood pressure. For example, PT transport stimulation by insulin may be involved in the pathogenesis of hypertension associated with insulin resistance. Type 1 angiotensin (Ang) II receptors in PT are critical for blood pressure homeostasis. Paradoxically, the effects of Ang II on PT transport are known to be biphasic. Unlike in other species, however, Ang II is recently shown to dose-dependently stimulate human PT transport via nitric oxide/cGMP/ERK pathway, which may represent a novel therapeutic target in human hypertension. In this paper, we will review the physiological and pathophysiological roles of PT transport.

Details

Title
Roles of Renal Proximal Tubule Transport in Acid/Base Balance and Blood Pressure Regulation
Author
Nakamura, Motonobu; Shirai, Ayumi; Yamazaki, Osamu; Satoh, Nobuhiko; Suzuki, Masashi; Horita, Shoko; Yamada, Hideomi; Seki, George
Publication year
2014
Publication date
2014
Publisher
John Wiley & Sons, Inc.
ISSN
23146133
e-ISSN
23146141
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
1547924706
Copyright
Copyright © 2014 Motonobu Nakamura et al. Motonobu Nakamura et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.