[Role of nitric oxide in the regulation of arterial pressure and renal function].
Nitric oxide (NO) is produced by three isoforms of NO synthase which catalyze the oxidation of L-arginine. Endothelial and neuronal NO synthases are constitutive and activated by an increase of intracellular calcium concentration. Activity of the inducible NO synthase is implied in inflammatory processes and does not depend on intracellular calcium. In the vessels, NO induces an active vasodilatory tone. Inhibition of NO synthases by L-arginine analogs results in a long-lasting pressor effect with renal damage, which demonstrates the role of the NO in the control of blood pressure and renal function. A defect of NO synthesis by endothelial or renal cells could be involved in the pathogenesis of salt-sensitive hypertension whereas, in other forms of hypertension, vascular NO would have a compensatory role. In the kidney, NO regulates glomerular filtration by vasodilating the glomerular afferent and, to a lesser extent, efferent arterioles and by increasing the ultrafiltration coefficient (Kf). NO is implied in the relationship between renal perfusion pressure and natriuresis and alters the tubulo-glomerular retrocontrol. The effects of the glomerular induction of NO synthase are under evaluation in various models of glomerulonephritis.
Dussaule
J C
JC
Service de Physiologie, Hôpital Saint-Antoine, Paris.
Chatziantoniou
C
C
D000818:Animals; D001794:Blood Pressure / Q000502:physiology*; D006801:Humans; D007668:Kidney / Q000502:physiology*; D009569:Nitric Oxide / Q000502:physiology*
D009569:Nitric Oxide