Sympathetic activation by chemical stimulation of white adipose tissues in rats

Shi, Zhen; Chen, Weiwei; Xiong, Xiao-Qing; Han, Ying; Zhou, Ye-Bo; Zhang, Feng; Gao, Xing-Ya; Zhu, Guo‐Qing

doi:10.1152/japplphysiol.01164.2011

Cited by 49 publications

(107 citation statements)

References 39 publications

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“…The sympatho-excitatory reflex, AAR, is involved in the regulation of sympathetic activity and blood pressure. 17 In the present study, capsaicin-induced AAR was enhanced in OP (ON and OH) and the AAR enhancement effect was much greater in OH than ON. Chemical stimulation of the WAT increased plasma NE, renin, and Ang II levels in OH, suggesting that the enhanced AAR not only activates sympathetic nervous system but also increases the activity of renin-Ang system in OH.…”

Section: Discussionsupporting

confidence: 44%

“…The reflex with negative feedback is helpful for keeping BW stable and preventing obesity. 14,17 However, persistent increase in afferent signals from WAT in overweight and obesity results in excessive sympathetic activation, which increases peripheral resistance and contributes to the development of hypertension and related organ damage. Furthermore, enhanced sympathetic activity activates the renin-Ang system, which deteriorates hypertension.…”

Section: Discussionmentioning

confidence: 99%

“…AAR was evaluated by the RSNA and MAP responses to injections of capsaicin (1.0 nmol/μL) into 4 sites of right inguinal WAT (iWAT) at a rate of 4.0 μL/min for 2 minutes for each site. 17 The c-fos expression in the PVN was determined with immunohistochemistry. Plasma renin, angiotensin (Ang) II, and norepinephrine (NE) levels were determined with ELISA.…”

Section: Methodsmentioning

confidence: 99%

“…Chemical stimulation of WAT-induced sympatho-excitatory reflex is called AAR. 17 WAT denervation or chemical lesion of the neurons in paraventricular nucleus (PVN) abolished the AAR induced by chemical stimulation. These findings suggest that the AAR is involved in the regulation of sympathetic activity and blood pressure.…”

mentioning

confidence: 99%

“…These findings suggest that the AAR is involved in the regulation of sympathetic activity and blood pressure. 17 Neuroanatomical studies have shown sensory and efferent sympathetic innervations of WAT. [18][19][20][21] We hypothesize that the enhanced AAR may play an important role in the sympathetic activation and hypertension in obesity.…”

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confidence: 99%

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Enhanced Adipose Afferent Reflex Contributes to Sympathetic Activation in Diet-Induced Obesity Hypertension

et al. 2012

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It is known that sympathetic activity is significantly enhanced in obesity hypertension.1,2 Combined blockage of α-and β-receptors caused a greater decrease in blood pressure in obese hypertensive subjects than that in lean hypertensive subjects. 3 Autonomic ganglionic blockade induced a greater depressor response in obese rats than that in lean rats. 4 A greater depressor effect of ganglionic blocker was found in obese subjects than normal-weight subjects.5 Renal sympathetic denervation markedly attenuated sodium and water retention and hypertension in diet-induced obesity in dogs. 6 Excessive sympathetic activity plays a critical role in the pathogenesis and target organ complication of the obesity hypertension. [7][8][9] Muscle sympathetic nerve activity was more closely associated with the level of abdominal visceral fat than total fat mass or abdominal subcutaneous fat in obese humans.10 Fat in the abdominal viscera has a particularly strong effect on blood pressure.11 Central obesity is characterized by a greater sympathetic activation than that in peripheral obesity. 12Weight loss decreased the sympathetic activity in obese metabolic syndrome subjects. 13 These findings indicate that the increased abdominal visceral fat is an important factor contributing to sympathetic activation. The mechanisms involved in the sympathetic activation of obesity hypertension (OH) remain uncertain. However, some encouraging findings about the adipose afferent reflex (AAR) in our laboratory have shed light on revealing the neural mechanisms of sympathetic activation in OH. Injection of leptin into white adipose tissue (WAT) of rats increased the sympathetic outflow to the WAT, 14 brown adipose tissue, pancreas, liver, 15 and kidney. 16 We recently found that WAT injection of capsaicin, bradykinin, adenosine, or leptin increased renal sympathetic nerve activity (RSNA) and mean arterial pressure (MAP) in normal rats. WAT injection of capsaicin increased afferent nerve activity of the WAT and efferent nerve activity of both WAT and brown adipose tissue. Chemical stimulation of WAT-induced sympatho-excitatory reflex is called AAR.17 WAT denervation or chemical lesion of the neurons in paraventricular nucleus (PVN) abolished the AAR induced by chemical stimulation. These findings suggest that the AAR is involved in the regulation of sympathetic activity Abstract-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...

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Section: Discussionsupporting

confidence: 44%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Enhanced Adipose Afferent Reflex Contributes to Sympathetic Activation in Diet-Induced Obesity Hypertension

et al. 2012

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The Sympathetic Innervation of Adipose Tissues: Regulation, Functions, and Plasticity

Willows

Blaszkiewicz

Townsend

2023

Comprehensive Physiology

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The sympathetic nervous system (SNS) is a crucial arm of the peripheral nervous system (PNS) and includes catecholaminergic neurons that release norepinephrine (NE) onto numerous effector tissues and organs in the body. SNS innervation of both white (WAT) and brown adipose tissue (BAT) is clearly essential for proper tissue function and metabolic control, as decades of surgical, chemical, and genetic denervation studies have demonstrated. Despite our vast knowledge about adipose sympathetic innervation, especially in the context of cold-stimulated browning and thermogenesis that are under SNS control, newer data now provide a nuanced view of the SNS supply to adipose, including its regulation by local neuroimmune cells and neurotrophic factors, the co-release of modulatory neuropeptides along with NE, the importance of local SNS drive to adipose versus systemic increases in circulating catecholamines, and the long-overlooked interplay between adipose sympathetic and sensory nerves. This article brings a modern view to the regulation of sympathetic innervation patterns in WAT and BAT, how to image and quantify the nerve supply, contributions of adipose SNS to tissue functions, and how adipose tissue nerves respond to tissue remodeling and plasticity with changing energy demands.

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SOD1 gene transfer into paraventricular nucleus attenuates hypertension and sympathetic activity in spontaneously hypertensive rats

Yuan

Zhang

et al. 2012

Pflugers Arch - Eur J Physiol

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Excessive sympathetic activity contributes to the initiation and progression of hypertension. Reactive oxygen species in the paraventricular nucleus (PVN) is involved in sympathetic overdrive and hypertension. The present study was designed to investigate whether superoxide dismutase 1 (SOD1) overexpression in the PVN attenuated sympathetic activation and hypertension. Adenoviral vectors containing human SOD1 or null adenoviral vectors were microinjected into the PVN of Wistar rats and spontaneously hypertensive rats (SHR). Significant depressor effects were observed from weeks 1 to 4 after SOD1 gene transfer in SHR. Acute experiments were carried out at the end of the 3rd week. In the PVN, superoxide anion and angiotensin II levels were increased while SOD1 activity and protein expression were decreased in SHR, which were attenuated by SOD1 overexpression in the PVN. However, SOD1 overexpression had no significant effect on the SOD2 activity in the PVN. The blood pressure response to ganglionic blockade, cardiac sympathetic nerve activity, and cardiac sympathetic afferent reflex (CSAR) were enhanced, and the plasma norepinephrine level was increased in SHR, which were prevented by SOD1 gene transfer in the PVN. Furthermore, SOD1 overexpression decreased the ratio of left ventricular weight to body weight, cross-sectional areas of myocardial cells, media thickness, and the media/lumen ratio of small arteries in the heart in SHR. These results indicate that SOD1 overexpression in the PVN reduces arterial blood pressure, attenuates excessive sympathetic activity and CSAR, and improves myocardial and vascular remodeling in SHR.

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Sympathetic activation by chemical stimulation of white adipose tissues in rats

Cited by 49 publications

References 39 publications

Enhanced Adipose Afferent Reflex Contributes to Sympathetic Activation in Diet-Induced Obesity Hypertension

Enhanced Adipose Afferent Reflex Contributes to Sympathetic Activation in Diet-Induced Obesity Hypertension

The Sympathetic Innervation of Adipose Tissues: Regulation, Functions, and Plasticity

SOD1 gene transfer into paraventricular nucleus attenuates hypertension and sympathetic activity in spontaneously hypertensive rats

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