Hypertension and chronic renal failure is a highly prevalent combination, which greatly increases cardiovascular morbidity and mortality. Substantial evidence indicates that sympathetic nervous system (SNS) overactivity may play an important role. In rats with 5/6 nephrectomy, norepinephrine turnover rate increases in brain nuclei involved in noradrenergic blood pressure control, whereas dorsal rhizotomy prevents hypertension. In humans, increased peripheral SNS activity, with normalization of SNS activity after nephrectomy has been documented. Renal injuries may activate renal afferent pathways that connect with integrative brain structures involved in SNS activity and blood pressure regulation. Local increased cerebral production of angiotensin II and subsequent activation of oxidative stress may lead to decreased production of nitric oxide and mediate SNS activation...