V.M. Campese, N. Mitra, D. Sandee Kidney International

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Hypertension in renal parenchymal disease: Why is it so resistant to treatment? V.M. Campese, N. Mitra, D. Sandee Kidney International Volume 69, Issue 6, Pages 967-973 (March 2006) DOI: 10.1038/sj.ki.5000177 Copyright © 2006 International Society of Nephrology Terms and Conditions

Figure 1 This schema summarizes current concepts linking renal damage with increased sympathetic nervous system (SNS) activity. Renal damage/ischemia stimulates afferent pathways, which integrate with key brain structures involved in the noradrenergic control of blood pressure. The central mediator of this pathway appears to be angiotensin II, which stimulates SNS activity through specific angiotensin-1 (AT1) receptors. Specific blockers of these receptors abrogate central SNS activation mediated by renal injury. Efferent SNS pathways may cause hypertension and contribute to cardiovascular and renal damage. Kidney International 2006 69, 967-973DOI: (10.1038/sj.ki.5000177) Copyright © 2006 International Society of Nephrology Terms and Conditions