| | Renal nerves play a key role in the crosstalk between the kidneys and the CNS to control blood pressure and body fluid composition. We showed that increased sodium-hydrogen exchanger isoform3 (NHE3) activity induced by renal nerve stimulation depends on the activation of the angiotensin (Ang) II type 1 (AT1) receptor by Ang II under physiological conditions. Moreover, it is known that the increased sympathetic nerve activity to the kidney and the renal afferent nerve activity to the CNS may contribute to the outcome of diseases, such as hypertension and chronic kidney disease. Renal denervation has shown promising results for the treatment of resistant hypertensive patients and chronic kidney disease, however, the underlying mechanisms of renal denervation are not completely understood. In a renovascular model of hypertension, we showed that the activity of RVLM and PVN sympathetic premotor neurons triggered by angiotensin II and oxidative stress is a major mechanism involved in the maintenance of sympathoexcitation of the cardiovascular system. Recent studies by our group have shown that renal denervation leads to central changes in 2 kidney, 1 clip rats and reduces sympathetic drive to other targets in renovascular hypertension model and 5/6 nephrectomy model of chronic kidney disease.
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