Role of nitric oxide in regulation of the renal medulla in normal and hypertensive kidneys. Curr Opin Nephrol Hypertens 2002 Jan;11(1):93-8
Date
12/26/2001Pubmed ID
11753093DOI
10.1097/00041552-200201000-00014Scopus ID
2-s2.0-0036140854 (requires institutional sign-in at Scopus site) 44 CitationsAbstract
Accumulating evidence favors the notion that perfusion of the medulla of the kidney is regulated through the effects of nitric oxide. Reduction of nitric oxide production in the medulla by local tissue infusion of nitric oxide synthase blockers leads to reduction of medullary blood flow, salt retention and hypertension. Conversely, infusion of L-arginine to increase nitric oxide abrogates hypertension and enhances medullary blood flow in animal models. Nitric oxide levels can also be controlled through its consumption by reactive oxygen species. Thus, medullary oxidative stress might influence blood pressure and sodium balance through changes in nitric oxide. Nitric oxide inhibits sodium chloride reabsorption by the thick ascending limb and collecting duct. The likelihood that some forms of hypertension result directly from pathological alteration of transporters, channels, regulatory elements or enzymes that affect medullary nitric oxide seems high.
Author List
Pallone TL, Mattson DLMESH terms used to index this publication - Major topics in bold
AnimalsHumans
Hypertension
Kidney Medulla
Nitric Oxide
Reactive Oxygen Species
Reference Values
Renal Circulation
Sodium
