Hypertension in chronic renal failure is very common and contributes to the
morbidity, mortality and progression of renal disease. The pathogenesis of
hypertension in chronic renal failure has mostly been attributed to sodium
retention and to activation of the renin-angiotensin-aldosterone system. M
ore recently, an abundance of evidence has accumulated to support a role fo
r increased sympathetic nervous system activity in the genesis of hypertens
ion associated with chronic renal failure. Evidence from our laboratory has
also demonstrated that the rise in central sympathetic nervous system acti
vity is mitigated by increased local expression of nitric oxide synthase mR
NA and NOx production. The upregulation of nitric oxide production in the b
rain is mediated by interleukin-1beta. Thus, interleukin-1 beta may stimula
te local nitric oxide production in the brain and mitigate the rise in symp
athetic nervous system activity and in blood pressure observed in rats with
chronic renal failure, Curr Opin Nephrol Hypertens 8:213-216. (C) 1999 Lip
pincott Williams & Wilkins.