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Specific Afferent Renal Denervation Prevents Reduction in Neuronal Nitric Oxide Synthase Within the Paraventricular Nucleus in Rats With Chronic Heart Failure.
Hypertension. 2018 09; 72(3):667-675.H

Abstract

Renal denervation (RDN) has been shown to restore endogenous neuronal nitric oxide synthase (nNOS) in the paraventricular nucleus (PVN) and reduce sympathetic drive during chronic heart failure (CHF). The purpose of the present study was to assess the contribution of afferent renal nerves to the nNOS-mediated sympathetic outflow within the PVN in rats with CHF. CHF was induced in rats by ligation of the left coronary artery. Four weeks after surgery, selective afferent RDN (A-RDN) was performed by bilateral perivascular application of capsaicin on the renal arteries. Seven days after intervention, nNOS protein expression, nNOS immunostaining signaling, and diaphorase-positive stained cells were significantly decreased in the PVN of CHF rats, changes that were reversed by A-RDN. A-RDN reduced basal lumbar sympathetic nerve activity in rats with CHF (8.5%±0.5% versus 17.0%±1.2% of max). Microinjection of nNOS inhibitor L-NMMA (L-NG-monomethyl arginine citrate) into the PVN produced a blunted increase in lumbar sympathetic nerve activity in rats with CHF. This response was significantly improved after A-RDN (Δ lumbar sympathetic nerve activity: 25.7%±2.4% versus 11.2%±0.9%). Resting afferent renal nerves activity was substantially increased in CHF compared with sham rats (56.3%±2.4% versus 33.0%±4.7%). These results suggest that intact afferent renal nerves contribute to the reduction of nNOS in the PVN. A-RDN restores nNOS and thus attenuates the sympathoexcitation. Also, resting afferent renal nerves activity is elevated in CHF rats, which may highlight a crucial neural mechanism arising from the kidney in the maintenance of enhanced sympathetic drive in CHF.

Authors+Show Affiliations

From the Division of Basic Biomedical Sciences, Sanford School of Medicine of the University of South Dakota, Vermillion (H.Z., X.L.).Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha (K.K., K.P.P.).From the Division of Basic Biomedical Sciences, Sanford School of Medicine of the University of South Dakota, Vermillion (H.Z., X.L.).Department of Pharmacology and Physiology, St. Louis University School of Medicine, MO (M.M.K.).Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha (K.K., K.P.P.).

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

30012866

Citation

Zheng, Hong, et al. "Specific Afferent Renal Denervation Prevents Reduction in Neuronal Nitric Oxide Synthase Within the Paraventricular Nucleus in Rats With Chronic Heart Failure." Hypertension (Dallas, Tex. : 1979), vol. 72, no. 3, 2018, pp. 667-675.
Zheng H, Katsurada K, Liu X, et al. Specific Afferent Renal Denervation Prevents Reduction in Neuronal Nitric Oxide Synthase Within the Paraventricular Nucleus in Rats With Chronic Heart Failure. Hypertension. 2018;72(3):667-675.
Zheng, H., Katsurada, K., Liu, X., Knuepfer, M. M., & Patel, K. P. (2018). Specific Afferent Renal Denervation Prevents Reduction in Neuronal Nitric Oxide Synthase Within the Paraventricular Nucleus in Rats With Chronic Heart Failure. Hypertension (Dallas, Tex. : 1979), 72(3), 667-675. https://doi.org/10.1161/HYPERTENSIONAHA.118.11071
Zheng H, et al. Specific Afferent Renal Denervation Prevents Reduction in Neuronal Nitric Oxide Synthase Within the Paraventricular Nucleus in Rats With Chronic Heart Failure. Hypertension. 2018;72(3):667-675. PubMed PMID: 30012866.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Specific Afferent Renal Denervation Prevents Reduction in Neuronal Nitric Oxide Synthase Within the Paraventricular Nucleus in Rats With Chronic Heart Failure. AU - Zheng,Hong, AU - Katsurada,Kenichi, AU - Liu,Xuefei, AU - Knuepfer,Mark M, AU - Patel,Kaushik P, PY - 2018/7/18/pubmed PY - 2019/4/10/medline PY - 2018/7/18/entrez KW - heart failure KW - nitric oxide synthase KW - paraventricular hypothalamic nucleus KW - visceral afferent SP - 667 EP - 675 JF - Hypertension (Dallas, Tex. : 1979) JO - Hypertension VL - 72 IS - 3 N2 - Renal denervation (RDN) has been shown to restore endogenous neuronal nitric oxide synthase (nNOS) in the paraventricular nucleus (PVN) and reduce sympathetic drive during chronic heart failure (CHF). The purpose of the present study was to assess the contribution of afferent renal nerves to the nNOS-mediated sympathetic outflow within the PVN in rats with CHF. CHF was induced in rats by ligation of the left coronary artery. Four weeks after surgery, selective afferent RDN (A-RDN) was performed by bilateral perivascular application of capsaicin on the renal arteries. Seven days after intervention, nNOS protein expression, nNOS immunostaining signaling, and diaphorase-positive stained cells were significantly decreased in the PVN of CHF rats, changes that were reversed by A-RDN. A-RDN reduced basal lumbar sympathetic nerve activity in rats with CHF (8.5%±0.5% versus 17.0%±1.2% of max). Microinjection of nNOS inhibitor L-NMMA (L-NG-monomethyl arginine citrate) into the PVN produced a blunted increase in lumbar sympathetic nerve activity in rats with CHF. This response was significantly improved after A-RDN (Δ lumbar sympathetic nerve activity: 25.7%±2.4% versus 11.2%±0.9%). Resting afferent renal nerves activity was substantially increased in CHF compared with sham rats (56.3%±2.4% versus 33.0%±4.7%). These results suggest that intact afferent renal nerves contribute to the reduction of nNOS in the PVN. A-RDN restores nNOS and thus attenuates the sympathoexcitation. Also, resting afferent renal nerves activity is elevated in CHF rats, which may highlight a crucial neural mechanism arising from the kidney in the maintenance of enhanced sympathetic drive in CHF. SN - 1524-4563 UR - https://www.unboundmedicine.com/medline/citation/30012866/Specific_Afferent_Renal_Denervation_Prevents_Reduction_in_Neuronal_Nitric_Oxide_Synthase_Within_the_Paraventricular_Nucleus_in_Rats_With_Chronic_Heart_Failure_ L2 - http://www.ahajournals.org/doi/full/10.1161/HYPERTENSIONAHA.118.11071?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -