Nitric oxide (NO) is an endogenous vasodilator and antithrombogenic agent. NO appears to play an important role in renal physiology and pathophysiology. Under physiological conditions, NO participates in regulation of the glomerular microcirculation by modulating afferent arteriolar tone and relaxation of the mesangium. NO also may contribute to the regulation of renal sodium excretion and renin release. Endothelial dysfunction induced by a variety of injurious mechanisms can lead to decreased synthesis and release of renal NO. Within the glomerulus, a decrease in NO synthesis and/or release will favor thrombogenesis in the luminal side of the endothelium and may result in an imbalance in the regulation of vascular "tone," leading to a prevalence of vasoconstrictor substances such as angiotensin II and endothelin. Furthermore, the antiproliferative action of NO may modulate the proliferation of mesangial cells in response to a variety of inflammatory processes that affect the glomeruli. In Gram-negative sepsis, NO, synthesized in increased amounts by the inducible NO synthase, protects the glomerular circulation by maintaining renal perfusion and preventing glomerular thrombosis.
|Original language||English (US)|
|Issue number||5 SUPPL.|
|State||Published - May 1993|
- Nitric oxide
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine