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Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Hypertension 2016 ; 68 (1): 175-84 Nephropedia Template TP
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Renal Denervation Improves Exaggerated Sympathoexcitation in Rats with Heart Failure: A Role for nNOS in the Paraventricular Nucleus #MMPMID27185748
Patel KP; Xu B; Liu X; Sharma NM; Zheng H
Hypertension 2016[Jul]; 68 (1): 175-84 PMID27185748show ga
Renal denervation (RDN) has been postulated to reduce sympathetic drive during heart failure (HF), but the central mechanisms are not completely understood. The purpose of the present study was to assess the contribution of neuronal nitric oxide synthase (nNOS) within the paraventricular nucleus (PVN) in modulating sympathetic outflow in rats with HF that underwent RDN. HF was induced in rats by ligation of the left coronary artery. Four weeks after surgery, bilateral RDN was performed. Rats with HF had an increase in FosB-positive cells in the PVN with a concomitant increase in urinary excretion of norepinephrine and both of these parameters were ameliorated after RDN. nNOS-positive cells immunostaining, diaphorase staining, and nNOS protein expression were significantly decreased in the PVN of HF rats, findings that were ameliorated by RDN. Microinjection of nNOS inhibitor L-NMMA into the PVN resulted in a blunted increase in lumbar sympathetic nerve activity (?LSNA: 11 ± 2 vs. 24 ± 2%) in HF than in sham group. This response was normalized after RDN. Stimulation of afferent renal nerve (ARN) produced a greater activation of PVN neurons in rats with HF. ARN stimulation elicited a greater increase in LSNA in rats with HF compared to sham rats (?LSNA: 45 ± 5 vs. 22 ± 2%). These results suggest that intact renal nerves contribute to the reduction of nNOS in the PVN, resulting in activation of the neurons in the PVN of rats with HF. RDN restores nNOS and thus attenuates the sympathoexcitation commonly observed in HF.