Nitric oxide (NO) is intimately involved in the regulation of vascular
tone, renal haemodynamics and sodium balance. The physiological actio
ns of NO suggest important vascular and renal protective roles for NO.
When produced in large amounts, however, NO may also mediate cytotoxi
c effects. Increasing evidence suggests that endothelial function, not
ably the NO pathway may be compromised in hypertension. It is not know
n, however, whether changes in endothelial function are primary or sec
ondary to the development of hypertension. In renal diseases evidence
for both excessive and deficient activity of NO pathway has been found
. Increased glomerular production of NO via inducible NO synthase (NOS
) with potential cytotoxic consequences has been demonstrated in exper
imental acute glomerulonephritis. On the other hand, indirect evidence
obtained by means of NOS inhibitors point out to an important renopro
tective role for NO in renal diseases. NO may counteract disease progr
ession in renal diseases by preventing glomerular microthrombi, mainta
ining renal perfusion and medullary oxygenation, and via its anti-infl
ammatory/antiproliferative effects. However, these beneficial effects
of NO may be compromised (endothelial and/or tubular dysfunction) in c
hronic nephropathies resulting in an accelerated course of renal disea
se. In future, more specific inhibitors and activators of different NO
S isoforms are needed to elucidate the role of NO in various renal dis
eases in detail, and for treatment strategies aimed at modifying the N
O pathway.