SAGE-Hindawi Access to Research International Journal of Hypertension Volume 2011, Article ID 814354, 6 pages doi:10.4061/2011/814354 Review Article Sympathetic Renal Innervation and Resistant Hypertension Vito M. Campese,1 Elaine Ku,1 and Jeanie Park2 1 Division of Nephrology, USC/Keck School of Medicine, University of Southern California, 2020 Zonal Aveue, Los Angeles, CA 90033, USA 2 Renal Division, Department of Medicine, Emory University, Atlanta, GA, USA Correspondence should be addressed to Vito M. Campese, campese@usc.edu Received 1 September 2010; Accepted 1 November 2010 Academic Editor: Konstantinos Tsiouﬁs Copyright © 2011 Vito M. Campese et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Hypertension in chronic renal disease and renovascular disease is often resistant to therapy. Understanding the pathogenic mechanisms responsible for hypertension in these conditions may lead to improved and more targeted therapeutic interventions. Several factors have been implicated in the pathogenesis of hypertension associated with renal disease and/or renal failure. Although the role of sodium retention, total body volume expansion, and hyperactivity of the renin-angiotensin-aldosterone system (RAAS) are well recognized, increasing evidence suggests that aﬀerent impulses from the injured kidney may increase sympathetic nervous system activity in areas of the brain involved in noradrenergic regulation of blood pressure and contribute to the development and maintenance of hypertension associated with kidney disease. Recognition of this important pathogenic factor suggests that antiadrenergic drugs should be an essential component to the management of hypertension in patients with kidney disease, particularly those who are resistant to other modalities of therapy. 1. Hypertension Resistant to Therapy in Patients with Renovascular Disease and with Chronic Kidney Disease Although the majority of patients with resistant hyper- tension have essential hypertension, secondary forms of hypertension are more commonly seen in patients with resistant hypertension. Among the most common causes of secondary hypertension are renovascular hypertension and hypertension secondary to chronic kidney disease (CKD). Renovascular hypertension accounts for 2-3% of patients with hypertension and is often diﬃcult to control. Reno- vascular disease is present in 30% of patients with grade 3 or 4 hypertensive retinopathy [1]. In one study, 16.7% of clinically selected patients had renovascular hypertension, as documented by blood pressure response to correction of renal artery stenosis or removal of the involved kidney [2]. Hypertension is very prevalent among patients with CKD and it contributes to the high prevalence of cardio- vascular disease and progression of kidney disease in these patients (Table 1) [3–6]. Hypertension associated with renal parenchymal disease constitutes approximately 5% of all forms of hypertension, and it becomes more frequent as patient progress toward end-stage renal disease (ESRD). Nearly 85% of ESRD patients have hypertension. Hyper- tension is the single most important predictor of coronary artery disease in ESRD patients, even more so than other known cardiovascular risk factors [7]. Often, treatment of hypertension in ESRD patients is diﬃcult and inadequate. Understanding the mechanisms of hypertension may help improve therapy in such patient populations. 2. Evidence for Activation of the Sympathetic Nervous System (SNS) in Renovascular Hypertension and Kidney Disease The renin-angiotensin-aldosterone system (RAAS) plays a key role in blood pressure (BP) elevation in the early phase of renovascular hypertension. Later on, other mechanisms such as sodium retention and activation of the sympathetic nervous system (SNS) may contribute to hypertension [8, 9]. In one study, sixty-ﬁve patients with hypertension and renovascular disease demonstrated by angiography underwent measurements of plasma renin activity and