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.
ASJC Scopus subject areas
- Internal Medicine