Faculty Collaboration Database

Production and functional roles of nitric oxide in the proximal tubule. Am J Physiol Regul Integr Comp Physiol 2000 May;278(5):R1117-24

Date

05/09/2000

Pubmed ID

10801277

DOI

10.1152/ajpregu.2000.278.5.R1117

Scopus ID

2-s2.0-4243479783 (requires institutional sign-in at Scopus site)   115 Citations

Abstract

A significant role for nitric oxide (NO) in proximal tubule physiology and pathophysiology has been revealed by a series of in vivo and in vitro studies. Whether the proximal tubule produces NO under basal conditions is still controversial; however, evidence suggests that the proximal tubule is constantly exposed to NO that might include NO from nonproximal tubule sources. When challenged with a variety of stimuli, including hypoxia, the proximal tubule is able to produce large quantities of NO. In vivo studies generally indicate that NO inhibits fluid and sodium reabsorption by the proximal tubule. However, the final effect of NO on proximal tubular reabsorption appears to depend on the concentration of NO and involve interaction with other regulatory mechanisms. NO regulates Na(+)-K(+)-ATPase, Na(+)/H(+) exchangers, and paracellular permeability of proximal tubular cells, which may contribute to its effect on proximal tubular transport. Enhanced production of NO, perhaps depending on macrophage type inducible NO synthase, participates in hypoxic/ischemic proximal tubular injury. In conclusion, NO plays a fundamental role in both physiology and pathophysiology of the proximal tubule.

Author List

Liang M, Knox FG

MESH terms used to index this publication - Major topics in bold

Absorption
Animals
Humans
Ischemia
Kidney Tubules, Proximal
Nitric Oxide
Reperfusion Injury
Sodium