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

Hypertension is very common in patients with chronic renal failure (CRF) an d it contributes to morbidity and mortality as well as to the progression o f renal disease. Several mechanisms may play a role in the pathogenesis of hypertension iu CRF, but the best known are sodium retention and activation of the renin-angiotensin-aldosterone system. More recently, evidence has a ccumulated to support a role for increased sympathetic nervous system (SNS) activity in the genesis of hypertension associated with CRF. Our laborator y finding indicate that specific renal injuries, caused by 5/6 nephrectomy and/or phenol injection in the kidney, activate renal afferent pathways tha t connect with integrative structures in the brain involved in the regulati on of SNS activity and blood pressure. This results in a rise in blood pres sure sustained by noradrenergic mechanisms. Our laboratory has also shown that the rise in central SNS activity is miti gated by increased local expression of nitric oxide synthase (NOS)-mRNA and nitric oxide (NO) production, and by upregulation of interleukin-1 beta.