Enhanced angiotensin II-mediated central sympathoexcitation in streptozotocin-induced diabetes: role of superoxide anion

Patel, Kaushik P.; Mayhan, William G.; Bidasee, Keshore R.; Zheng, Hong

doi:10.1152/ajpregu.00246.2010

Cited by 32 publications

(32 citation statements)

References 46 publications

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“…This implied a deficit in the reflex residing either in the heart or within central pathways. These findings closely corresponded with observations in rat models of cardiac failure induced by coronary artery ligation (19) that the reflex regulation of renal sympathetic nerve activity by both the high-and low-pressure baroreceptors was blunted.…”

supporting

confidence: 89%

Impact of l-NAME on the cardiopulmonary reflex in cardiac hypertrophy

Buckley

Johns

2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Buckley MM, Johns EJ. Impact of L-NAME on the cardiopulmonary reflex in cardiac hypertrophy. Am J Physiol Regul Integr Comp Physiol 301: R1549 -R1556, 2011. First published August 24, 2011 doi:10.1152/ajpregu.00307.2011There is evidence that in cardiac failure, there is defective baroreceptor reflex control of sympathetic nerve activity. Often, cardiac failure is preceded by a state of cardiac hypertrophy in which there may be enhanced performance of the heart. This study investigated whether in two different models of cardiac hypertrophy, there was an increased contribution of nitric oxide (NO) to the low-pressure baroreceptor regulation of renal sympathetic nerve activity (RSNA) and nerve-dependent excretory function. Administration of a volume load, 0.25% body wt/min saline for 30 min, in normal rats decreased RSNA by 40% and increased urine flow by some 9-fold. Following nitro-L-arginine methyl ester (L-NAME) administration, 10 g·kg Ϫ1 ·min Ϫ1 for 60 min, which had no effect on blood pressure, heart rate, or RSNA, the volume loadinduced renal sympathoinhibitory and excretory responses were markedly enhanced. In cardiac hypertrophy states induced by 2 wk of isoprenaline/caffeine or 1 wk thyroxine administration, the volume challenge failed to suppress RSNA, and there were blunted increases in urine flow in the innervated kidneys, but following L-NAME infusion, the volume load decreased RSNA by 30 -40% and increased urine flow by some 20-fold in the innervated kidneys, roughly to the same extent as observed in normal rats. These findings suggest that the blunted renal sympathoinhibition and nerve-dependent diuresis to the volume load in cardiac hypertrophy are related to a heightened production or activity of NO within either the afferent or central arms of the reflex. renal sympathetic nerve activity; urine flow; nitric oxide CARDIAC HYPERTROPHY, DEFINED as an increase in the size and/or thickness of the ventricles in the heart, frequently progresses into heart failure (2) and is an independent predictor of cardiovascular morbidity and mortality (5,14). The development of cardiac hypertrophy is associated with an increased workload and an activation of the sympathetic nervous system, which drives the heart to ensure an adequate cardiac output and, if prolonged, may progress into cardiac failure. In the kidney, the raised sympathetic outflow will cause an enhanced sodium retention and raised circulatory volume, which will also contribute to the increased load on the heart (10).The reflex control of the cardiovascular system and blood pressure depends not only on arterial baroreceptors, but also on receptors located in the cardiopulmonary region. It is generally recognized that increasing circulatory volume leads to a fall in renal sympathetic nerve activity (RSNA), and vice versa, and has been termed the cardiopulmonary reflex. Interestingly, in two models of cardiac hypertrophy induced by isoprenaline/ caffeine or thyroxine exposure, it was found that the reflex renal sympathoinhibition in response to an ac...

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supporting

confidence: 89%

Impact of l-NAME on the cardiopulmonary reflex in cardiac hypertrophy

Buckley

Johns

2011

American Journal of Physiology-Regulatory, Integrative and Comp

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“…3). It is possible that Ang II-NADPH oxidase-superoxide may also affect other site(s) of the arterial baroreflex arc to blunt the arterial baroreflex in the diabetic state (such as central neural areas because enhanced Ang II-NADPH oxidase-superoxide signal is found in the paraventricular nucleus from STZ-induced diabetic rats (17)). It will be clarified in further study.…”

Section: Discussionmentioning

confidence: 99%

“…Patel, et al . have reported that elevation of the Ang II in the paraventricular nucleus induces the increase of sympathoexcitation in diabetes through triggering the superoxide production (17). Our previous studies have demonstrated that elevation of local Ang II level in the nodose ganglia can blunt the membrane excitability of the aortic baroreceptor neurons via NADPH oxidase-derived superoxide in the type 1 diabetes (14, 18).…”

Section: Introductionmentioning

confidence: 99%

Elevated Angiotensin II in Rat Nodose Ganglia Primes Diabetes-Blunted Arterial Baroreflex Sensitivity: Involvement of NADPH Oxidase Derived Superoxide

Li¹

2011

J Diabetes Metab

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Clinical trials and experimental animal studies have confirmed the contribution of arterial baroreflex impairment in causing excess morbidity and mortality in type-1 diabetes. Our previous study has shown that angiotensin II (Ang II)-NADPH oxidase-superoxide signaling is associated with the reduced cell excitability in the aortic baroreceptor neurons (a primary afferent limb of the arterial baroreflex) from diabetic rats. In this study, we examined whether above-mentioned signaling might contribute to the blunted baroreflex sensitivity in streptozotocin-induced diabetic rats. Using Ang II 125I radioimmunoassay and lucigenin chemiluminescence method, we found Ang II concentration, NADPH oxidase activity, and superoxide production in the nodose ganglia were enhanced in diabetic rats, compared to sham rats. As an index of the arterial baroreflex sensitivity, the reflex decreases in blood pressure and heart rate evoked by unilateral steady-frequency aortic depressor nerve stimulation were attenuated in diabetic rats. Local microinjection (50 nl) of losartan (an AT1 receptor antagonist, 1 nmol), apocynin (a NADPH oxidase inhibitor, 1 nmol), and tempol (a superoxide dismutase mimetic, 10 nmol) into the nodose ganglia significantly improved the arterial baroreflex sensitivity in diabetic rats. In addition, these three chemicals also normalized exogenous Ang II-attenuated arterial baroreflex sensitivity in sham rats. These results indicate that overactivation of the Ang II-NADPH oxidase-superoxide signal pathway in the nodose ganglia contributes to the blunted baroreflex sensitivity in diabetes.

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“…Interestingly ang-II increases the production of superoxide anion via stimulation of NAD(P)H oxidase, and the resulting oxidative stress has been postulated as an important mediator of ang-II signaling, in the central nervous system. A study on rats has shown that ang-II activates sympathetic outflow by stimulation of superoxide anion in the paraventricular nucleus [Patel et al, 2011]. Thus ang-II is a possible important link between the pulmonary and cardiovascular effects of PM mediated by the autonomic nervous system.…”

Section: Evidence For the Autonomic Nervous System And Ros Participatmentioning

confidence: 99%

Air Pollution, Reactive Oxygen Species (ROS), and Autonomic Nervous System Interactions Modulate Cardiac Oxidative Stress and Electrophysiological Changes

Ghelfi¹

2011

Advanced Topics in Environmental Health and Air Pollution Case Studies

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Enhanced angiotensin II-mediated central sympathoexcitation in streptozotocin-induced diabetes: role of superoxide anion

Cited by 32 publications

References 46 publications

Impact of l-NAME on the cardiopulmonary reflex in cardiac hypertrophy

Impact of l-NAME on the cardiopulmonary reflex in cardiac hypertrophy

Elevated Angiotensin II in Rat Nodose Ganglia Primes Diabetes-Blunted Arterial Baroreflex Sensitivity: Involvement of NADPH Oxidase Derived Superoxide

Air Pollution, Reactive Oxygen Species (ROS), and Autonomic Nervous System Interactions Modulate Cardiac Oxidative Stress and Electrophysiological Changes

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