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Murray D Esler - One of the best experts on this subject based on the ideXlab platform.
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central and peripheral Sympathetic Activation in heart failure
Cardiovascular Research, 2021Co-Authors: Guido Grassi, Giuseppe Mancia, Murray D EslerAbstract:The Sympathetic nervous system overdrive occurring in heart failure has been reported since more than half a century. Refinements in the methodological approaches to assess human Sympathetic neural function have allowed during recent years to better define various aspects related to the neuroadrenergic alteration. These include 1) the different participation of the individual regional Sympathetic cardiovascular districts at the process, 2) the role of the central nervous system in determining the neuroadrenergic overdrive, 3) the involvement of baroreflex, cardiopulmonary reflex and chemoreflex mechanisms in the phoenomenon, which is also closely linked to inflammation and the immune reaction, 4) the relationships with the severity of the disease, its ischaemic or idiopathic nature and the preserved or reduced left ventricular ejection fraction and 5) the adverse functional and structural impact of the Sympathetic Activation on cardiovascular organs, such as the brain, the heart and the kidneys. Information have been also gained on the active role exerted by the Sympathetic Activation on the disease outcome and its potential relevance as target of the therapeutic interventions based on non-pharmacological, pharmacological and invasive approaches, including the renal denervation, the splanchnic Sympathetic nerve ablation and the carotid baroreflex stimulation. The still undefined aspects of the neurogenic alterations and the unmet goals of the therapeutic approach having the Sympathetic Activation as a target of the intervention will be finally mentioned.
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peripheral chemoreflex Activation contributes to Sympathetic baroreflex impairment in chronic heart failure
Journal of Hypertension, 2012Co-Authors: Fabien Despas, Elisabeth Lambert, Gavin W Lambert, Angelica Vaccaro, M Labrunee, Nicolas Franchitto, Marine Lebrin, Michel Galinier, J M Senard, Murray D EslerAbstract:Background:Chemoreflex-mediated Sympathetic Activation contributes to both initiation and progression of chronic heart failure (CHF).Method:To study the direct role of increased peripheral chemosensitivity in reducing Sympathetic baroreflex function in CHF patients, we compared Sympathetic barorefle
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effects of renal denervation on Sympathetic Activation blood pressure and glucose metabolism in patients with resistant hypertension
Frontiers in Physiology, 2012Co-Authors: Markus P Schlaich, Elisabeth Lambert, Dagmara Hering, Paul A Sobotka, Henry Krum, Gavin W Lambert, Murray D EslerAbstract:Increased central Sympathetic drive is a hallmark of several important clinical conditions including essential hypertension, heart failure, chronic kidney disease, and insulin resistance. Afferent signaling from the kidneys has been identified as an important contributor to elevated central Sympathetic drive and increased Sympathetic outflow to the kidney and other organs is crucially involved in cardiovascular control. While the resultant effects on renal hemodynamic parameters, sodium and water retention, and renin release are particularly relevant for both acute and long term regulation of blood pressure, increased Sympathetic outflow to other vascular beds may facilitate further adverse consequences of sustained Sympathetic Activation such as insulin resistance, which is commonly associated with hypertension. Recent clinical studies using catheter-based radiofrequency ablation technology to achieve functional renal denervation in patients with resistant hypertension have identified the renal nerves as therapeutic target and have helped to further expose the Sympathetic link between hypertension and insulin resistance. Initial data from two clinical trials and several smaller mechanistic clinical studies indicate that this novel approach may indeed provide a safe and effective treatment alternative for resistant hypertension and some of its adverse consequences.
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Sympathetic Activation in chronic renal failure
Journal of The American Society of Nephrology, 2009Co-Authors: Markus P Schlaich, Flora Socratous, Sarah Hennebry, Nina Eikelis, Elisabeth Lambert, Nora E Straznicky, Murray D Esler, Gavin LambertAbstract:The potential involvement of Sympathetic overactivity has been neglected in this population despite accumulating experimental and clinical evidence suggesting a crucial role of Sympathetic Activation for both progression of renal failure and the high rate of cardiovascular events in patients with chronic kidney disease. The contribution of Sympathetic neural mechanisms to the occurrence of cardiac arrhythmias, the development of hypertension, and the progression of heart failure are well established; however, the exact mechanisms contributing to heightened Sympathetic tone in patients with chronic kidney disease are unclear. This review analyses potential mechanisms underlying Sympathetic Activation in chronic kidney disease, the range of adverse consequences associated with this Activation, and potential therapeutic implications resulting from this relationship.
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mediators of Sympathetic Activation in metabolic syndrome obesity
Current Hypertension Reports, 2008Co-Authors: Nora E Straznicky, Nina Eikelis, Elisabeth Lambert, Murray D EslerAbstract:The metabolic syndrome represents a major public health burden because of its high prevalence in the general population and its association with cardiovascular disease and type 2 diabetes. Accumulated evidence based on biochemical, neurophysiologic, and indirect measurements of autonomic activity indicate that visceral obesity and the metabolic syndrome are associated with enhanced Sympathetic neural drive and vagal impairment. The mechanisms linking metabolic syndrome with Sympathetic Activation are complex and not completely understood, and cause-effect relationships need further clarification from prospective trials. Components of the metabolic syndrome that may directly or indirectly enhance Sympathetic drive include hyperinsulinemia, leptin, nonesterified fatty acids, proinflammatory cytokines, angiotensinogen, baroreflex impairment, and obstructive sleep apnea. β-Adrenoceptor polymorphisms have also been associated with adrenoceptor desensitization, increased adiposity, insulin resistance, and enhanced Sympathetic activity. Because chronic Sympathetic Activation contributes to hypertension and its target-organ damage, sympatho-inhibition remains an important goal in the therapeutic management of the metabolic syndrome.
Giuseppe Mancia - One of the best experts on this subject based on the ideXlab platform.
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central and peripheral Sympathetic Activation in heart failure
Cardiovascular Research, 2021Co-Authors: Guido Grassi, Giuseppe Mancia, Murray D EslerAbstract:The Sympathetic nervous system overdrive occurring in heart failure has been reported since more than half a century. Refinements in the methodological approaches to assess human Sympathetic neural function have allowed during recent years to better define various aspects related to the neuroadrenergic alteration. These include 1) the different participation of the individual regional Sympathetic cardiovascular districts at the process, 2) the role of the central nervous system in determining the neuroadrenergic overdrive, 3) the involvement of baroreflex, cardiopulmonary reflex and chemoreflex mechanisms in the phoenomenon, which is also closely linked to inflammation and the immune reaction, 4) the relationships with the severity of the disease, its ischaemic or idiopathic nature and the preserved or reduced left ventricular ejection fraction and 5) the adverse functional and structural impact of the Sympathetic Activation on cardiovascular organs, such as the brain, the heart and the kidneys. Information have been also gained on the active role exerted by the Sympathetic Activation on the disease outcome and its potential relevance as target of the therapeutic interventions based on non-pharmacological, pharmacological and invasive approaches, including the renal denervation, the splanchnic Sympathetic nerve ablation and the carotid baroreflex stimulation. The still undefined aspects of the neurogenic alterations and the unmet goals of the therapeutic approach having the Sympathetic Activation as a target of the intervention will be finally mentioned.
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Sympathetic nerve traffic Activation in essential hypertension and its correlates systematic reviews and meta analyses
Hypertension, 2018Co-Authors: Guido Grassi, Gino Seravalle, Fosca Quartitrevano, Anna Pisano, Davide Bolignano, Graziella Darrigo, Francesca Mallamaci, Carmine Zoccali, Giuseppe ManciaAbstract:Muscle Sympathetic nerve activity (MSNA) has shown that Sympathetic Activation may occur in essential hypertension (EHT). However, the small sample size of the studies, the heterogeneity of the patients examined, and the presence of confounders represented major weaknesses not allowing to draw definite conclusions. Among the 432 studies identified providing information in EHT on MSNA, 63 were eligible (1216 patients) and meta-analyzed grouping them on the basis of clinically relevant questions: (1) Is MSNA increased in hypertension of mild/moderate-to-severe degree? (2) Does Sympathetic Activation occur in borderline, white-coat, and masked EHT? (3) Is MSNA related to clinic and ambulatory blood pressure and target organ damage? (4) Are heart rate and venous plasma norepinephrine valuable surrogate markers of MSNA in clinical practice? The results show that MSNA was significantly greater (1.5×; P P r =0.67 and r =0.83; P r =−0.38; P r =0.28; P r =0.27; P
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marked Sympathetic Activation and baroreflex dysfunction in true resistant hypertension
International Journal of Cardiology, 2014Co-Authors: Guido Grassi, Gianmaria Brambilla, Gino Seravalle, Claudio Pini, M Alimento, Rita Facchetti, Domenico Spaziani, Cesare Cuspidi, Giuseppe ManciaAbstract:Abstract Background An increase in Sympathetic drive to the heart and the peripheral circulation characterizes mild and severe essential hypertension. However, it remains unsettled whether Sympathetic cardiovascular influences are potentiated in true resistant hypertension (RHT). Methods In 32 RHT patients treated with 4.6±0.3 drugs (mean±SEM) and aged 58.6±2.1years, 35 non-resistant treated hypertensives (HT) and 19 normotensive controls (NT), all age-matched with RHT, we measured clinic, 24-hour ambulatory and beat-to-beat blood pressures (BP), heart rate (HR, EKG), muscle Sympathetic nerve traffic (MSNA, microneurography) and spontaneous baroreflex MSNA-sensitivity. Results BP values were markedly greater in RHT patients than in NT and HT (172.2±1.7/100.7±1.2 vs 132.1±1.3/82.1±0.9 and 135.5±1.2/83.6±0.9mmHg, P 0 . 01 ). This was paralleled by a significant and marked increase in MSNA (87.8±2.0 vs 46.8±2.6 and 59.3±1.7 and bursts/100 heartbeats, P 0 . 01 ). In multiple regression analysis the MSNA increase observed in RHT was significantly related to hemodynamic, hormonal and metabolic variables. It was also significantly related to plasma aldosterone values as well as spontaneous baroreflex MSNA-sensitivity, which were the variables that at the multivariate analysis were more closely related to the adrenergic Activation of RHT after adjustment for confounders, including antihypertensive treatment (r 2 partial =0.04405 and r 2 partial =0.00878, P 0 . 05 for both). Conclusions These data represent the first evidence that RHT is a state of marked adrenergic overdrive, greater for magnitude than that detectable in HT. They also suggest that impaired baroreflex mechanisms, along with hemodynamic and neurohumoral factors, may be responsible for the phenomenon.
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Sympathetic Activation in cardiovascular and renal disease
Journal of Nephrology, 2009Co-Authors: Guido Grassi, Francesca Arenare, Federico Pieruzzi, Gianmaria Brambilla, Giuseppe ManciaAbstract:Given the importance of adrenergic neural functioning in cardiovascular control, the hypothesis that an elevation in Sympathetic drive represents a key pathophysiological feature of diseases characterized by an impairment in cardiac or renal function has been long considered. However, modern approaches to directly quantify Sympathetic nerve firing in humans have only been possible in the last 2 decades to provide objective documentation for the hypothesis. This paper will review the evidence that conditions such as essential hypertension, congestive heart failure and metabolic syndrome are all accompanied by an increased Sympathetic drive, which is likely in all of them to play a pathogenetic role. It will then offer examples showing that Sympathetic influences are directly involved in the progression of organ damage associated with these conditions. Finally, evidence will be presented that a maximum degree of Sympathetic Activation can be seen in end-stage renal failure, in which a relationship between Sympathetic Activation and clinical outcome has been documented. This has therapeutic implications, which involve the need to use treatments that oppose rather than enhance Sympathetic neural Activation.
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excessive Sympathetic Activation in heart failure with obesity and metabolic syndrome characteristics and mechanisms
Hypertension, 2007Co-Authors: Guido Grassi, Gino Seravalle, Fosca Quartitrevano, F Scopelliti, Raffaella Delloro, Gianbattista Bolla, Giuseppe ManciaAbstract:Congestive heart failure is characterized by Sympathetic Activation, which has also been described in the metabolic syndrome. No information exists, however, as to whether the sympathostimulating effects of these 2 conditions summate when heart failure is complicated by the metabolic syndrome, leading to an exceedingly high adrenergic drive. This is clinically relevant, because in heart failure Sympathetic Activation is closely related to mortality. We studied 48 control subjects (age: 58.4±1.6 years, mean±SEM) and 89 age-matched heart failure patients (New York Heart Association class II), of whom 47 were without and 42 were with metabolic syndrome. Measurements included blood pressure (Finapres), heart rate (ECG), and Sympathetic nerve traffic (microneurography) at rest and during baroreceptor manipulation. Waist circumference, blood pressure, and metabolic variables were greater in heart failure with metabolic syndrome than in heart failure without metabolic syndrome and in control subjects. Left ventricular ejection fraction and end-diastolic diameter were similarly altered in the 2 heart failure groups. Compared with control subjects, Sympathetic nerve activity was greater in heart failure patients without metabolic syndrome (64.7±3.2 versus 45.8±2.9 bursts/100 heartbeats; P P
Guido Grassi - One of the best experts on this subject based on the ideXlab platform.
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central and peripheral Sympathetic Activation in heart failure
Cardiovascular Research, 2021Co-Authors: Guido Grassi, Giuseppe Mancia, Murray D EslerAbstract:The Sympathetic nervous system overdrive occurring in heart failure has been reported since more than half a century. Refinements in the methodological approaches to assess human Sympathetic neural function have allowed during recent years to better define various aspects related to the neuroadrenergic alteration. These include 1) the different participation of the individual regional Sympathetic cardiovascular districts at the process, 2) the role of the central nervous system in determining the neuroadrenergic overdrive, 3) the involvement of baroreflex, cardiopulmonary reflex and chemoreflex mechanisms in the phoenomenon, which is also closely linked to inflammation and the immune reaction, 4) the relationships with the severity of the disease, its ischaemic or idiopathic nature and the preserved or reduced left ventricular ejection fraction and 5) the adverse functional and structural impact of the Sympathetic Activation on cardiovascular organs, such as the brain, the heart and the kidneys. Information have been also gained on the active role exerted by the Sympathetic Activation on the disease outcome and its potential relevance as target of the therapeutic interventions based on non-pharmacological, pharmacological and invasive approaches, including the renal denervation, the splanchnic Sympathetic nerve ablation and the carotid baroreflex stimulation. The still undefined aspects of the neurogenic alterations and the unmet goals of the therapeutic approach having the Sympathetic Activation as a target of the intervention will be finally mentioned.
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Sympathetic nerve traffic Activation in essential hypertension and its correlates systematic reviews and meta analyses
Hypertension, 2018Co-Authors: Guido Grassi, Gino Seravalle, Fosca Quartitrevano, Anna Pisano, Davide Bolignano, Graziella Darrigo, Francesca Mallamaci, Carmine Zoccali, Giuseppe ManciaAbstract:Muscle Sympathetic nerve activity (MSNA) has shown that Sympathetic Activation may occur in essential hypertension (EHT). However, the small sample size of the studies, the heterogeneity of the patients examined, and the presence of confounders represented major weaknesses not allowing to draw definite conclusions. Among the 432 studies identified providing information in EHT on MSNA, 63 were eligible (1216 patients) and meta-analyzed grouping them on the basis of clinically relevant questions: (1) Is MSNA increased in hypertension of mild/moderate-to-severe degree? (2) Does Sympathetic Activation occur in borderline, white-coat, and masked EHT? (3) Is MSNA related to clinic and ambulatory blood pressure and target organ damage? (4) Are heart rate and venous plasma norepinephrine valuable surrogate markers of MSNA in clinical practice? The results show that MSNA was significantly greater (1.5×; P P r =0.67 and r =0.83; P r =−0.38; P r =0.28; P r =0.27; P
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marked Sympathetic Activation and baroreflex dysfunction in true resistant hypertension
International Journal of Cardiology, 2014Co-Authors: Guido Grassi, Gianmaria Brambilla, Gino Seravalle, Claudio Pini, M Alimento, Rita Facchetti, Domenico Spaziani, Cesare Cuspidi, Giuseppe ManciaAbstract:Abstract Background An increase in Sympathetic drive to the heart and the peripheral circulation characterizes mild and severe essential hypertension. However, it remains unsettled whether Sympathetic cardiovascular influences are potentiated in true resistant hypertension (RHT). Methods In 32 RHT patients treated with 4.6±0.3 drugs (mean±SEM) and aged 58.6±2.1years, 35 non-resistant treated hypertensives (HT) and 19 normotensive controls (NT), all age-matched with RHT, we measured clinic, 24-hour ambulatory and beat-to-beat blood pressures (BP), heart rate (HR, EKG), muscle Sympathetic nerve traffic (MSNA, microneurography) and spontaneous baroreflex MSNA-sensitivity. Results BP values were markedly greater in RHT patients than in NT and HT (172.2±1.7/100.7±1.2 vs 132.1±1.3/82.1±0.9 and 135.5±1.2/83.6±0.9mmHg, P 0 . 01 ). This was paralleled by a significant and marked increase in MSNA (87.8±2.0 vs 46.8±2.6 and 59.3±1.7 and bursts/100 heartbeats, P 0 . 01 ). In multiple regression analysis the MSNA increase observed in RHT was significantly related to hemodynamic, hormonal and metabolic variables. It was also significantly related to plasma aldosterone values as well as spontaneous baroreflex MSNA-sensitivity, which were the variables that at the multivariate analysis were more closely related to the adrenergic Activation of RHT after adjustment for confounders, including antihypertensive treatment (r 2 partial =0.04405 and r 2 partial =0.00878, P 0 . 05 for both). Conclusions These data represent the first evidence that RHT is a state of marked adrenergic overdrive, greater for magnitude than that detectable in HT. They also suggest that impaired baroreflex mechanisms, along with hemodynamic and neurohumoral factors, may be responsible for the phenomenon.
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Sympathetic Activation in cardiovascular and renal disease
Journal of Nephrology, 2009Co-Authors: Guido Grassi, Francesca Arenare, Federico Pieruzzi, Gianmaria Brambilla, Giuseppe ManciaAbstract:Given the importance of adrenergic neural functioning in cardiovascular control, the hypothesis that an elevation in Sympathetic drive represents a key pathophysiological feature of diseases characterized by an impairment in cardiac or renal function has been long considered. However, modern approaches to directly quantify Sympathetic nerve firing in humans have only been possible in the last 2 decades to provide objective documentation for the hypothesis. This paper will review the evidence that conditions such as essential hypertension, congestive heart failure and metabolic syndrome are all accompanied by an increased Sympathetic drive, which is likely in all of them to play a pathogenetic role. It will then offer examples showing that Sympathetic influences are directly involved in the progression of organ damage associated with these conditions. Finally, evidence will be presented that a maximum degree of Sympathetic Activation can be seen in end-stage renal failure, in which a relationship between Sympathetic Activation and clinical outcome has been documented. This has therapeutic implications, which involve the need to use treatments that oppose rather than enhance Sympathetic neural Activation.
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excessive Sympathetic Activation in heart failure with obesity and metabolic syndrome characteristics and mechanisms
Hypertension, 2007Co-Authors: Guido Grassi, Gino Seravalle, Fosca Quartitrevano, F Scopelliti, Raffaella Delloro, Gianbattista Bolla, Giuseppe ManciaAbstract:Congestive heart failure is characterized by Sympathetic Activation, which has also been described in the metabolic syndrome. No information exists, however, as to whether the sympathostimulating effects of these 2 conditions summate when heart failure is complicated by the metabolic syndrome, leading to an exceedingly high adrenergic drive. This is clinically relevant, because in heart failure Sympathetic Activation is closely related to mortality. We studied 48 control subjects (age: 58.4±1.6 years, mean±SEM) and 89 age-matched heart failure patients (New York Heart Association class II), of whom 47 were without and 42 were with metabolic syndrome. Measurements included blood pressure (Finapres), heart rate (ECG), and Sympathetic nerve traffic (microneurography) at rest and during baroreceptor manipulation. Waist circumference, blood pressure, and metabolic variables were greater in heart failure with metabolic syndrome than in heart failure without metabolic syndrome and in control subjects. Left ventricular ejection fraction and end-diastolic diameter were similarly altered in the 2 heart failure groups. Compared with control subjects, Sympathetic nerve activity was greater in heart failure patients without metabolic syndrome (64.7±3.2 versus 45.8±2.9 bursts/100 heartbeats; P P
Xiaoqing Xiong - One of the best experts on this subject based on the ideXlab platform.
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cardiac Sympathetic afferent reflex and its implications for Sympathetic Activation in chronic heart failure and hypertension
Acta Physiologica, 2015Co-Authors: Weiwei Chen, Qi Chen, Xiaoqing Xiong, Yuehua Li, Yu-ming KangAbstract:Persistent excessive Sympathetic Activation greatly contributes to the pathogenesis of chronic heart failure (CHF) and hypertension. Cardiac Sympathetic afferent reflex (CSAR) is a sympathoexcitatory reflex with positive feedback characteristics. Humoral factors such as bradykinin, adenosine and reactive oxygen species produced in myocardium due to myocardial ischaemia stimulate cardiac Sympathetic afferents and thereby reflexly increase Sympathetic activity and blood pressure. The CSAR is enhanced in myocardial ischaemia, CHF and hypertension. The enhanced CSAR at least partially contributes to the Sympathetic Activation and pathogenesis of these diseases. Nucleus of the solitary tract (NTS), hypothalamic paraventricular nucleus (PVN) and rostral ventrolateral medulla are the most important central sites involved in the modulation and integration of the CSAR. Angiotensin II, AT1 receptors and NAD(P)H oxidase-derived superoxide anions pathway in the PVN are mainly responsible for the enhanced CSAR in CHF and hypertension. Central angiotensin-(1-7), nitric oxide, endothelin, intermedin, hydrogen peroxide and several other signal molecules are involved in regulating CSAR. Blockade of the CSAR shows beneficial effects in CHF and hypertension. This review focuses on the anatomical and physiological basis of the CSAR, the interaction of CSAR with baroreflex and chemoreflex, and the role of enhanced CSAR in the pathogenesis of CHF and hypertension.
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apelin 13 and apj in paraventricular nucleus contribute to hypertension via Sympathetic Activation and vasopressin release in spontaneously hypertensive rats
Acta Physiologica, 2014Co-Authors: Feng Zhang, Jue-jin Wang, Qi Chen, Yu-ming Kang, Xiaoqing Xiong, Haijian Sun, Xingya Gao, Guo-qing ZhuAbstract:Aims Apelin is a specific endogenous ligand of orphan G protein-coupled receptor APJ. This study was designed to determine the roles and mechanisms of apelin-13 and APJ in paraventricular nucleus (PVN) in renal Sympathetic nerve activity (RSNA), arginine vasopressin (AVP) release and mean arterial pressure (MAP) in spontaneously hypertensive rats (SHR). Method Acute experiment was carried out in 13-week-old male SHR and Wistar-Kyoto rats (WKY) under anaesthesia. RSNA and MAP responses to the PVN microinjection were determined. Apelin and APJ expressions were examined with quantitative real-time PCR and Western blot. AVP and noradrenaline were determined with ELISA. Osmotic minipumps were used for chronic PVN infusion in conscious WKY. Results Apelin and APJ in the PVN were up-regulated in SHR. The PVN microinjection of apelin-13 increased, but APJ antagonist F13A decreased the RSNA, MAP, plasma noradrenaline and AVP levels in SHR. N-methyl-D-aspartate receptor (NMDAR) antagonist plus non-NMDAR antagonist abolished the apelin-13-induced Sympathetic Activation rather than AVP release. NMDAR antagonist or non-NMDAR antagonist alone attenuated the apelin-13-induced Sympathetic Activation. Chronic infusion of apelin-13 into the PVN in normotensive rats induced hypertension, increased plasma noradrenaline and AVP levels and promoted myocardial atrial natriuretic peptide and beta-myosin heavy chain mRNA expressions, two indicative markers of cardiac hypertrophy. Conclusion Apelin-13 and APJ in the PVN contribute to hypertension via Sympathetic Activation and AVP release in SHR. The sympatho-excitatory effect of apeline-13 is mediated by both NMDAR and non-NMDAR in the PVN. Persistent Activation of APJ in the PVN induces hypertension.
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adipose afferent reflex Sympathetic Activation and obesity hypertension
Acta Physiologica, 2014Co-Authors: Xiaoqing Xiong, Weiwei ChenAbstract:: Excessive Sympathetic activity contributes to the pathogenesis of hypertension and the progression of the related organ damage. Adipose afferent reflex (AAR) is a sympatho-excitatory reflex that the afferent activity from white adipose tissue (WAT) increases Sympathetic outflow and blood pressure. Hypothalamic paraventricular nucleus (PVN or PVH) is one of the central sites in the control of the AAR, and ionotropic glutamate receptors in the nucleus mediate the AAR. The AAR is enhanced in obesity and obesity hypertension. Enhanced WAT afferent activity and AAR contribute to the excessive Sympathetic Activation and hypertension in obesity. Blockage of the AAR attenuates the excessive Sympathetic activity and hypertension. Leptin may be one of sensors in the WAT for the AAR, and is involved in the enhanced AAR in obesity and hypertension. This review focuses on the neuroanatomical basis and physiological functions of the AAR, and the important role of the enhanced AAR in the pathogenesis of obesity hypertension.
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enhanced adipose afferent reflex contributes to Sympathetic Activation in diet induced obesity hypertension
Hypertension, 2012Co-Authors: Xiaoqing Xiong, Weiwei Chen, Yebo Zhou, Feng ZhangAbstract:We recently found that adipose afferent reflex (AAR) induced by chemical stimulation of white adipose tissue (WAT) increased Sympathetic outflow and blood pressure in normal rats. The study was designed to test the hypothesis that AAR contributes to Sympathetic Activation in obesity hypertension. Male rats were fed with a control diet (12% kcal as fat) or high-fat diet (42% kcal as fat) for 12 weeks to induce obesity hypertension. Stimulation of WAT with capsaicin increased renal Sympathetic nerve activity and mean arterial pressure. Both AAR and WAT afferent activity were enhanced in obesity hypertension (OH) compared with obesity nonhypertension (ON) and in ON compared with obesity-resistant or control diet rats. WAT sensory denervation induced by resiniferatoxin caused greater decreases in renal Sympathetic nerve activity and mean arterial pressure in OH than ON and in ON than obesity-resistant or control. The depressor effect of resiniferatoxin lasted ≥3 weeks in OH. Leptin antagonist in WAT reduced renal Sympathetic nerve activity and mean arterial pressure in OH. WAT injection of capsaicin increased plasma renin, angiotensin II, and norepinephrine levels in OH and caused more c-fos expression in paraventricular nucleus in OH than ON and in ON than obesity-resistant or control rats. Inhibiting paraventricular nucleus neurons with lidocaine attenuated renal Sympathetic nerve activity in OH and ON, decreased mean arterial pressure in OH, and abolished the capsaicin-induced AAR in all groups. The results indicate that enhanced AAR contributes to Sympathetic Activation in OH, and paraventricular nucleus plays an important role in the enhanced AAR and Sympathetic Activation in OH.
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involvement of enhanced cardiac Sympathetic afferent reflex in Sympathetic Activation in early stage of diabetes
Journal of Applied Physiology, 2012Co-Authors: Lei Zhang, Xiaoqing XiongAbstract:Cardiac Sympathetic afferent reflex (CSAR) is involved in Sympathetic Activation. The present study was designed to investigate the contribution of enhanced CSAR to Sympathetic Activation in the ea...
Wei De - One of the best experts on this subject based on the ideXlab platform.
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superoxide anions in the paraventricular nucleus mediate the enhanced cardiac Sympathetic afferent reflex and Sympathetic activity in renovascular hypertensive rats
Journal of Applied Physiology, 2011Co-Authors: Ning Yuan, Wei DeAbstract:An enhanced cardiac Sympathetic afferent reflex (CSAR) is involved in the Sympathetic Activation in renovascular hypertension. The present study was designed to determine the role of superoxide ani...
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angiotensin at1 receptors in paraventricular nucleus contribute to Sympathetic Activation and enhanced cardiac Sympathetic afferent reflex in renovascular hypertensive rats
Experimental Physiology, 2011Co-Authors: Ai-dong Chen, Shujuan Zhang, Ning Yuan, Yao Xu, Wei DeAbstract:Sympathetic activity is enhanced in hypertension, which contributes to the pathogenesis of hypertension and progression of organ damage. The cardiac Sympathetic afferent reflex (CSAR) is enhanced in renovascular hypertension and involved in the Sympathetic Activation. The present study was designed to investigate whether angiotensin II (Ang II) and Ang II type 1 (AT1) receptors in paraventricular nucleus (PVN) contribute to the enhanced CSAR and Sympathetic outflow in experimental renovascular hypertensive rats. Hypertension was induced by the two-kidney one-clip (2K1C) method. The normotensive rats underwent sham operation (Sham). Acute experimentation was carried out at the end of the 4th week. Under urethane and α-chloralose anaesthesia, the renal Sympathetic nerve activity (RSNA) and mean arterial pressure (MAP) were recorded in rats with sino-aortic denervation and cervical vagotomy. The AT1 receptor expression was determined with Western blot. The CSAR was evaluated by the response of RSNA and MAP to epicardial application of 1.0 nmol of capsaicin. The AT1 receptor expression in the PVN was increased, and Ang II in the PVN augmented the enhanced CSAR and RSNA in 2K1C rats. The effects of Ang II were abolished by pretreatment with the AT1 receptor antagonist, losartan, in 2K1C rats. Losartan in the PVN normalized the enhanced CSAR and decreased the RSNA and MAP in 2K1C rats. These results indicate that the increased activity of AT1 receptors in the PVN contributes to the enhanced CSAR and excessive Sympathetic Activation in renovascular hypertensive rats.
