Department of Medicine, Division of Nephrology, University of Southern California Medical Center, Los Angeles, California, USA

Correspondence: Vito M. Campese, M.D., Division of Nephrology, LAC/USC Medical Center, 1200 North State Street, Los Angeles, CA 90033, USA. E-mail: campese@hsc.usc.edu

Abstract

Neurogenic factors and hypertension in renal disease. Hypertension in chronic renal failure (CRF) is very common and contributes to morbidity and mortality and to the progression of renal disease. The pathogenesis of hypertension in CRF has been attributed mostly 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 (SNS) activity in the genesis of hypertension associated with CRF. Evidence from our laboratory has also demonstrated that the rise in central SNS activity is mitigated by increased local expression 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.