The kidney and the neurogenic control of blood pressure in renal disease

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. More recently, an abundance of evidence has accumulated to support a role for increased sympathetic nervous system activity in the genesis of hypertension associated with chronic renal failure. Evidence from our laboratory has also demonstrated that the rise in central sympathetic nervous system activity is mitigated by increased local expression of nitric oxide synthase mRNA and NOx production. The upregulation of nitric oxide production in the brain is mediated by interleukin-1beta. Thus, interleukin-1 beta may stimulate local nitric oxide production in the brain and mitigate the rise in sympathetic nervous system activity and in blood pressure observed in rats with chronic renal failure.