Regulation of renal NaCl transport by nitric oxide, endothelin, and ATP: clinical implications.

Abstract:

:NaCl absorption along the nephron is regulated not just by humoral factors but also by factors that do not circulate or act on the cells where they are produced. Generally, nitric oxide (NO) inhibits NaCl absorption along the nephron. However, the effects of NO in the proximal tubule are controversial and may be biphasic. Similarly, the effects of endothelin on proximal tubule transport are biphasic. In more distal segments, endothelin inhibits NaCl absorption and may be mediated by NO. Adenosine triphosphate (ATP) inhibits sodium bicarbonate absorption in the proximal tubule, NaCl absorption in thick ascending limbs via NO, and water reabsorption in collecting ducts. Defects in the effects of NO, endothelin, and ATP increase blood pressure, especially in a NaCl-sensitive manner. In diabetes, disruption of NO-induced inhibition of transport may contribute to increased blood pressure and renal damage. However, our understanding of how NO, endothelin, and ATP work, and of their role in pathology, is rudimentary at best.

journal_name

Annu Rev Physiol

authors

Garvin JL,Herrera M,Ortiz PA

doi

10.1146/annurev-physiol-012110-142247

subject

Has Abstract

pub_date

2011-01-01 00:00:00

pages

359-76

eissn

0066-4278

issn

1545-1585

journal_volume

73

pub_type

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