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Exercise training improves endogenous nitric oxide mechanisms within the paraventricular nucleus in rats with heart failure.
Am J Physiol Heart Circ Physiol. 2005 May; 288(5):H2332-41.AJ

Abstract

Previously, we have demonstrated that an altered endogenous nitric oxide (NO) mechanism within the paraventricular nucleus (PVN) contributes to increased renal sympathetic nerve activity (RSNA) in heart failure (HF) rats. The goal of this study was to examine the effect of exercise training (ExT) in improving the endogenous NO mechanism within the PVN involved in the regulation of RSNA in rats with HF. ExT significantly restored the decreased number of neuronal NO synthase (nNOS)-positive neurons in the PVN (129 +/- 17 vs. 99 +/- 6). nNOS mRNA expression and protein levels in the PVN were also significantly increased in HF-ExT rats compared with HF-sedentary rats. To examine the functional role of NO within the PVN, an inhibitor of NOS, N(G)-monomethyl-L-arginine, was microinjected into the PVN. Dose-dependent increases in RSNA, arterial blood pressure (BP), and heart rate (HR) were produced in all rats. There was a blunted increase in these parameters in HF rats compared with the sham-operated rats. ExT significantly augmented RSNA responses in rats with HF (33% vs. 20% at the highest dose), thus normalizing the responses. The NO donor sodium nitroprusside, microinjected into the PVN, produced dose-dependent decreases in RSNA, BP, and HR in both sham and HF rats. ExT significantly improved the blunted decrease in RSNA in HF rats (36% vs. 17% at the highest dose). In conclusion, our data indicate that ExT improves the altered NO mechanism within the PVN and restores NO-mediated changes in RSNA in rats with HF.

Authors+Show Affiliations

Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska 68198-5850, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

15653768

Citation

Zheng, Hong, et al. "Exercise Training Improves Endogenous Nitric Oxide Mechanisms Within the Paraventricular Nucleus in Rats With Heart Failure." American Journal of Physiology. Heart and Circulatory Physiology, vol. 288, no. 5, 2005, pp. H2332-41.
Zheng H, Li YF, Cornish KG, et al. Exercise training improves endogenous nitric oxide mechanisms within the paraventricular nucleus in rats with heart failure. Am J Physiol Heart Circ Physiol. 2005;288(5):H2332-41.
Zheng, H., Li, Y. F., Cornish, K. G., Zucker, I. H., & Patel, K. P. (2005). Exercise training improves endogenous nitric oxide mechanisms within the paraventricular nucleus in rats with heart failure. American Journal of Physiology. Heart and Circulatory Physiology, 288(5), H2332-41.
Zheng H, et al. Exercise Training Improves Endogenous Nitric Oxide Mechanisms Within the Paraventricular Nucleus in Rats With Heart Failure. Am J Physiol Heart Circ Physiol. 2005;288(5):H2332-41. PubMed PMID: 15653768.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Exercise training improves endogenous nitric oxide mechanisms within the paraventricular nucleus in rats with heart failure. AU - Zheng,Hong, AU - Li,Yi-Fan, AU - Cornish,Kurt G, AU - Zucker,Irving H, AU - Patel,Kaushik P, Y1 - 2005/01/14/ PY - 2005/1/18/pubmed PY - 2005/6/1/medline PY - 2005/1/18/entrez SP - H2332 EP - 41 JF - American journal of physiology. Heart and circulatory physiology JO - Am J Physiol Heart Circ Physiol VL - 288 IS - 5 N2 - Previously, we have demonstrated that an altered endogenous nitric oxide (NO) mechanism within the paraventricular nucleus (PVN) contributes to increased renal sympathetic nerve activity (RSNA) in heart failure (HF) rats. The goal of this study was to examine the effect of exercise training (ExT) in improving the endogenous NO mechanism within the PVN involved in the regulation of RSNA in rats with HF. ExT significantly restored the decreased number of neuronal NO synthase (nNOS)-positive neurons in the PVN (129 +/- 17 vs. 99 +/- 6). nNOS mRNA expression and protein levels in the PVN were also significantly increased in HF-ExT rats compared with HF-sedentary rats. To examine the functional role of NO within the PVN, an inhibitor of NOS, N(G)-monomethyl-L-arginine, was microinjected into the PVN. Dose-dependent increases in RSNA, arterial blood pressure (BP), and heart rate (HR) were produced in all rats. There was a blunted increase in these parameters in HF rats compared with the sham-operated rats. ExT significantly augmented RSNA responses in rats with HF (33% vs. 20% at the highest dose), thus normalizing the responses. The NO donor sodium nitroprusside, microinjected into the PVN, produced dose-dependent decreases in RSNA, BP, and HR in both sham and HF rats. ExT significantly improved the blunted decrease in RSNA in HF rats (36% vs. 17% at the highest dose). In conclusion, our data indicate that ExT improves the altered NO mechanism within the PVN and restores NO-mediated changes in RSNA in rats with HF. SN - 0363-6135 UR - https://www.unboundmedicine.com/medline/citation/15653768/Exercise_training_improves_endogenous_nitric_oxide_mechanisms_within_the_paraventricular_nucleus_in_rats_with_heart_failure_ L2 - https://journals.physiology.org/doi/10.1152/ajpheart.00473.2004?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -