Hypertension in chronic renal failure (CRF) is very common and contributes
to morbidity and mortality and to the progression of renal disease. The pat
hogenesis of hypertension in CRF has been attributed mostly to sodium reten
tion and to activation of the renin-angiotensin-aldosterone system. More re
cently an abundance of evidence has accumulated to support a role for incre
ased sympathetic nervous system (SNS) activity in the genesis of hypertensi
on associated with CRF. Evidence from our laboratory has also demonstrated
that the rise in central SNS activity is mitigated by increased local expre
ssion of nitric oxide synthase (NOS)-mRNA and nitric oxide (NO) production,
and that the upregulation of NO production in the brain is mediated by IL-
1 beta.