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Lower urinary tract dysfunction reported in autonomic disorders 自主神经紊乱中下尿路功能障碍的报道。
IF 3.3 4区 医学 Q2 NEUROSCIENCES Pub Date : 2025-12-01 Epub Date: 2025-09-03 DOI: 10.1016/j.autneu.2025.103341
Ekawat Vichayanrat , Shiwen Koay , Claire Hentzen , Sarah Wright , Amit Batla , Sara Simeoni , Valeria Iodice , Jalesh N. Panicker
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引用次数: 0
Antihypertensive effects of the treatment with ATZ and losartan in L-NAME hypertensive rats ATZ联合氯沙坦治疗L-NAME型高血压大鼠的降压作用
IF 3.3 4区 医学 Q2 NEUROSCIENCES Pub Date : 2025-12-01 Epub Date: 2025-10-20 DOI: 10.1016/j.autneu.2025.103359
Roberto Braz Pontes, Paulo Ricardo Lopes, Débora S.A. Colombari, Patrícia M. De Paula, Eduardo Colombari, Carina A.F. Andrade, Laurival A. De Luca Jr, José V. Menani
Previous works suggest that hydrogen peroxide (H2O2), a reactive oxygen species, attenuates brain angiotensin II-mediated hypertension in rats. Moreover, the subcutaneous (s.c.) administration of 3-amino-1,2,4-triazole (ATZ), a catalase inhibitor that increases H2O2 availability, reduces hypertension and sympathetic activity simultaneously with an increase in angiotensinergic activity in spontaneously hypertensive rats (SHRs). It is not clear how much the increase in angiotensinergic activity affects the sympatho-inhibition and the antihypertensive effect of ATZ, and if this is specific for SHRs. The present study evaluated the effects of s.c. ATZ and losartan (angiotensin II AT1 antagonist), alone or combined for 7 days, on mean arterial pressure (MAP) in nitric oxide synthase-inhibited hypertensive rats (L-NAME model). In addition, angiotensinergic and sympathetic activities were also investigated using acute intravenous losartan and hexamethonium (ganglionic blocker) in the same rats. The treatment with ATZ + losartan s.c. reduced MAP slightly below to normotensive levels in L-NAME hypertensive rats (88 ± 8, vs. L-NAME + saline: 162 ± 7 mmHg), whereas s.c. losartan alone partially reduced MAP (133 ± 7 mmHg). The hypotensive responses produced by hexamethonium were reduced in rats treated with ATZ + losartan s.c. (−44 ± 12, vs. L-NAME + saline: −71 ± 6 mmHg), suggesting that the treatment with ATZ + losartan s.c. significantly reduced sympathetic activation in L-NAME-treated rats. These findings suggest that the combination of ATZ and losartan efficiently blocks sympathetic and angiotensinergic activation in L-NAME hypertensive rats, abolishing hypertension. Further research is necessary on the mechanisms of H2O2 and ATZ antihypertensive action.
先前的研究表明,过氧化氢(H2O2)是一种活性氧,可以减轻大鼠脑血管紧张素ii介导的高血压。此外,皮下(s.c)给药3-氨基-1,2,4-三唑(ATZ),过氧化氢酶抑制剂,增加H2O2可用性,降低高血压和交感神经活动,同时增加自发性高血压大鼠(SHRs)的血管紧张素能活性。目前尚不清楚血管紧张素能活性的增加在多大程度上影响ATZ的交感神经抑制和降压作用,以及这是否是SHRs特有的。本研究评估了s.c. ATZ和氯沙坦(血管紧张素II AT1拮抗剂)单独或联合使用7天对一氧化氮合酶抑制高血压大鼠(L-NAME模型)平均动脉压(MAP)的影响。此外,在同一大鼠急性静脉注射氯沙坦和六甲溴铵(神经节阻滞剂)时,还研究了血管紧张素能和交感神经活动。ATZ +氯沙坦s.c.治疗使L-NAME高血压大鼠的MAP略低于正常水平(88±8,vs. L-NAME +生理盐水:162±7 mmHg),而s.c.氯沙坦单独治疗则部分降低MAP(133±7 mmHg)。ATZ +氯沙坦s.c组大鼠的降压反应降低(- 44±12,而L-NAME +生理盐水:- 71±6 mmHg),表明ATZ +氯沙坦s.c组显著降低了L-NAME组大鼠的交感神经激活。提示ATZ联合氯沙坦可有效阻断L-NAME高血压大鼠交感神经和血管紧张素能的激活,消除高血压。H2O2和ATZ的降压作用机制有待进一步研究。
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引用次数: 0
Autonomic responses in children and adolescents with orthostatic syncope and presyncope: children are not small adults 儿童和青少年直立性晕厥和晕厥前期的自主神经反应:儿童不是小大人。
IF 3.3 4区 医学 Q2 NEUROSCIENCES Pub Date : 2025-12-01 Epub Date: 2025-09-08 DOI: 10.1016/j.autneu.2025.103340
V.-E.M. Lucci , C.L. Protheroe , C.A. Albaro , M.G. Lloyd , K. Armstrong , S. Franciosi , S. Sanatani , V.E. Claydon
Children and adolescents commonly experience orthostatic intolerance associated with impaired participation and quality of life. We aimed to characterize autonomic responses to provoked presyncope in children with recurrent presyncope/syncope and healthy adolescents.
We determined orthostatic tolerance (OT, time to presyncope [mins]) in 36 pediatric patients (age 15 ± 3 yrs., 26 female) with recurrent presyncope/syncope, and 17 asymptomatic controls (age 13 ± 3 yrs., 8 female), using a tilt test with graded lower body negative pressure. Cardiovascular parameters, forearm vascular resistance (FVR), mean middle cerebral artery velocity (MCAvmean), and breath-by-breath end tidal gases were continuously monitored. Responses to the Valsalva maneuver (VM), cerebral autoregulation, and cerebral reactivity to carbon dioxide were also determined.
OT was similar in pediatric patients (21 ± 1.5 min) and controls (20 ± 2.0 min, p = 0.74), but smaller than adult reference values (33.8 ± 0.8 min, p < 0.01). Tilting decreased systolic arterial pressure in pediatric patients (p = 0.009), but not pediatric controls (p = 0.12). Tilting decreased MCAvmean (p = 0.002) in pediatric patients, with impairments in cerebral autoregulation (p = 0.02) that were negatively correlated with OT (r = −0.322; p = 0.024). Both pediatric patients (+48.9 ± 8.0 %) and controls (+36.7 ± 14.7 %) had small FVR responses compared to adult reference data (+100 ± 12 %, p < 0.01). Blood pressure responses to the VM were abnormal in pediatric patients, with a lower nadir in mean arterial pressure (81.7 ± 2.0 mmHg) compared to pediatric controls (94.0 ± 2.8 mmHg, p = 0.001).
Pediatric patients with recurrent presyncope/syncope had impaired orthostatic cardiovascular and autoregulatory responses compared to pediatric controls. Sympathetically-mediated responses were small in children, underscoring the need for pediatric-specific standards for orthostatic cardiovascular control, and treatments targeting enhancement of vascular resistance in children with syncope.
儿童和青少年通常经历与参与和生活质量受损相关的直立性不耐受。我们的目的是表征复发性晕厥/晕厥前症儿童和健康青少年对诱发性晕厥前症的自主神经反应。我们测定了36例儿童患者(年龄15±3岁)的直立耐受性(OT,到晕厥前的时间[分钟])。26例女性)伴有复发性晕厥前期/晕厥,对照组17例(年龄13±3岁)。(8名女性),采用倾斜试验,下体负压分级。连续监测心血管参数、前臂血管阻力(FVR)、平均大脑中动脉流速(MCAvmean)和逐呼吸末潮气。对Valsalva动作(VM)的反应、大脑自动调节和大脑对二氧化碳的反应也进行了测定。儿科患者的OT(21±1.5 min)与对照组(20±2.0 min, p = 0.74)相似,但小于成人参考值(33.8±0.8 min, p平均值(p = 0.002),脑自动调节功能障碍(p = 0.02)与OT呈负相关(r = -0.322; p = 0.024)。与成人参考数据相比,儿童患者(+48.9±8.0 %)和对照组(+36.7±14.7%)的FVR反应较小(+100±12%,p
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引用次数: 0
Acute effects of vericiguat on urine excretion during baroreflex-mediated sympathetic arterial pressure regulation in male rats 在压力反射介导的交感动脉压力调节过程中,白荆对雄性大鼠尿液排泄的急性影响。
IF 3.3 4区 医学 Q2 NEUROSCIENCES Pub Date : 2025-12-01 Epub Date: 2025-11-19 DOI: 10.1016/j.autneu.2025.103363
Mika Nishikawa , Toru Kawada , Nana Hiraki , Masafumi Fukumitsu , Kei Sato , Hiroyuki Kinoshita , Shinji Kawahito , Keita Saku
Vericiguat is a soluble guanylate cyclase stimulator that acts via both nitric oxide-dependent and -independent mechanisms. Previously, we found that vericiguat decreases arterial pressure (AP) primarily by reducing systemic vascular resistance without significantly affecting sympathetic nerve activity. In this study, we investigated whether the AP reduction by vericiguat decreases urine excretion. In male Wistar–Kyoto rats (n = 8), the bilateral carotid sinus baroreceptor regions were isolated from the systemic circulation. The relationship between AP and urine excretion was examined during baroreflex-mediated AP changes before and during intravenous vericiguat administration (10 μg·kg−1·min−1). Vericiguat significantly decreased the operating point AP (104.6 ± 4.2 vs. 85.0 ± 4.1 mmHg, P = 0.008), primarily by decreasing the slope of the baroreflex peripheral arc. However, it maintained urine excretion at the operating point AP (55.5 ± 5.9 vs. 59.8 ± 6.9 μL·min−1·kg−1, P = 0.250) by significantly increasing the slope of the relationship between AP and normalized urine flow (0.53 ± 0.09 vs. 0.99 ± 0.14 μL·min−1·kg−1·mmHg−1, P = 0.008). The maintenance of urine excretion during vericiguat administration might be beneficial for patients with fluid retention.
Vericiguat是一种可溶性鸟苷酸环化酶刺激剂,通过一氧化氮依赖性和非依赖性机制起作用。先前,我们发现vericiguat降低动脉压(AP)主要是通过降低全身血管阻力而不显著影响交感神经活动。在这项研究中,我们研究了vericiguat减少AP是否会减少尿液排泄。雄性Wistar-Kyoto大鼠(n = 8)从体循环中分离出双侧颈动脉窦压力感受器区。在静脉给药(10 μg·kg-1·min-1)前和静脉给药期间,通过bar反射介导的AP变化,检测AP与尿排泄的关系。Vericiguat主要通过降低气压反射外周弧线的斜率而显著降低了工作点AP(104.6±4.2 vs 85.0±4.1 mmHg, P = 0.008)。然而,通过显著增加AP与正常尿流之间的斜率(0.53±0.09比0.99±0.14 μL·min-1·kg-1·mmHg-1, P = 0.008),它维持了操作点AP的尿量(55.5±5.9比59.8±6.9 μL·min-1·kg-1, P = 0.250)。在给药期间保持尿液排泄可能对液体潴留患者有益。
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引用次数: 0
Autonomic function testing and symptom severity in patients with suspected mast cell activation disorders 怀疑肥大细胞活化障碍患者的自主神经功能检测和症状严重程度。
IF 3.3 4区 医学 Q2 NEUROSCIENCES Pub Date : 2025-12-01 Epub Date: 2025-11-17 DOI: 10.1016/j.autneu.2025.103362
Amro M. Stino , Jodi Nelson , Olivia Gutgsell , Ahmed Eldokla , Jasmine Liu , Cem Akin
We assessed both objective and subjective measures of autonomic severity in patients with formally classified mast cell activation disorder (MCAD), hereditary alpha tryptasemia (HaT), and systemic mastocytosis. In all subjects, autonomic disease severity was objectively mild but subjectively moderate to severe. The presence of MCAD did not yield consistent differences on subjective or objective severity measures, although HaT did associate with lower objective (but not subjective) severity measures. In conclusion, assessment of MCAD and related disorders can be conducted using formal classification criteria, and in those with suspected dysautonomia, the workup should incorporate objective and subjective measures of dysautonomia.
我们评估了正式分类肥大细胞激活障碍(MCAD)、遗传性α -色氨酸血症(HaT)和全身性肥大细胞增多症患者自主神经严重程度的客观和主观测量。所有受试者的自主神经疾病严重程度客观上为轻度,主观上为中度至重度。MCAD的存在并没有在主观或客观的严重程度测量上产生一致的差异,尽管HaT确实与较低的客观(但不是主观)严重程度测量相关。综上所述,MCAD及相关疾病的评估可以使用正式的分类标准进行,对于怀疑有自主神经异常的患者,检查应结合自主神经异常的客观和主观测量。
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引用次数: 0
Sacral neuromodulation for low urinary tract dysfunction: overview and mechanisms of action 骶神经调节治疗低尿路功能障碍:综述和作用机制
IF 3.3 4区 医学 Q2 NEUROSCIENCES Pub Date : 2025-10-01 Epub Date: 2025-08-19 DOI: 10.1016/j.autneu.2025.103337
Pierre-Luc Dequirez , Stefan De Wachter , Xavier Biardeau

Objectives

Sacral neuromodulation (SNM) is widely used since the 1990's for overactive bladder (OAB) and non-obstructive urinary retention (NOUR) with good clinical results. Though, its mechanisms of action are not fully elucidated.

Materials and methods

This narrative review intends to explore the various hypotheses of mechanisms of action in SNM, and to propose a theoretical model of action based on the current literature.

Results

SNM may modulate afferent signaling primarily through sub-sensory activation of pelvic floor muscles, which in turn may generate afferent input transmitted via the spinal cord to supraspinal structures, rather than through direct afferent neural stimulation. SNM may restore the balance between the sympathetic nervous system (SNS) and parasympathetic nervous system (PSNS) by decreasing activity in the anterior cingulate cortex and increasing activity in the median prefrontal cortex. SNM may also modulate the activity of the limbic system (cingulate cortex, insula), that is related to emotions and is frequently dysregulated in Fowler's syndrome – a specific NOUR entity, and patients with OAB. In NOUR, SNM may restore the periaqueductal gray activity through a diminution of excessive inhibitory afferent messages, particularly through modification of the activity of the median prefrontal cortex. Finally, sacral neuromodulation (SNM) may influence neural plasticity at the peripheral, spinal, and/or supraspinal levels; however, the underlying mechanisms and specific neurophysiological changes remain incompletely understood.

Conclusion

While our understanding of the mechanisms of action of SNM is still evolving, emerging data point toward a multifaceted process involving modulation of peripheral afferent input, spinal processing, and supraspinal structures - including those involved in sensorimotor integration, emotional regulation, and autonomic balance.
目的骶神经调节(SNM)自20世纪90年代以来广泛应用于膀胱过动症(OAB)和非梗阻性尿潴留(NOUR)的治疗,取得了良好的临床效果。然而,其作用机制尚未完全阐明。材料与方法本文旨在探讨SNM中作用机制的各种假设,并在现有文献的基础上提出一个作用的理论模型。结果snm可能主要通过骨盆底肌的亚感觉激活来调节传入信号,而骨盆底肌的亚感觉激活可能产生经脊髓传递到棘上结构的传入输入,而不是通过直接的传入神经刺激来调节传入信号。SNM可能通过减少前扣带皮层的活动和增加正中前额皮质的活动来恢复交感神经系统(SNS)和副交感神经系统(PSNS)之间的平衡。SNM也可能调节边缘系统(扣带皮层、脑岛)的活动,这与情绪有关,在Fowler综合征(一种特殊的NOUR实体)和OAB患者中经常失调。在NOUR中,SNM可能通过减少过度抑制性传入信息来恢复导水管周围的灰色活动,特别是通过改变正中前额皮质的活动。最后,骶神经调节(SNM)可能影响周围、脊柱和/或脊柱上水平的神经可塑性;然而,潜在的机制和特定的神经生理变化仍然不完全清楚。虽然我们对SNM作用机制的理解仍在不断发展,但新出现的数据指向一个涉及外周传入输入、脊髓加工和棘上结构(包括那些涉及感觉运动整合、情绪调节和自主神经平衡的结构)调节的多方面过程。
{"title":"Sacral neuromodulation for low urinary tract dysfunction: overview and mechanisms of action","authors":"Pierre-Luc Dequirez ,&nbsp;Stefan De Wachter ,&nbsp;Xavier Biardeau","doi":"10.1016/j.autneu.2025.103337","DOIUrl":"10.1016/j.autneu.2025.103337","url":null,"abstract":"<div><h3>Objectives</h3><div>Sacral neuromodulation (SNM) is widely used since the 1990's for overactive bladder (OAB) and non-obstructive urinary retention (NOUR) with good clinical results. Though, its mechanisms of action are not fully elucidated.</div></div><div><h3>Materials and methods</h3><div>This narrative review intends to explore the various hypotheses of mechanisms of action in SNM, and to propose a theoretical model of action based on the current literature.</div></div><div><h3>Results</h3><div>SNM may modulate afferent signaling primarily through sub-sensory activation of pelvic floor muscles, which in turn may generate afferent input transmitted via the spinal cord to supraspinal structures, rather than through direct afferent neural stimulation. SNM may restore the balance between the sympathetic nervous system (SNS) and parasympathetic nervous system (PSNS) by decreasing activity in the anterior cingulate cortex and increasing activity in the median prefrontal cortex. SNM may also modulate the activity of the limbic system (cingulate cortex, insula), that is related to emotions and is frequently dysregulated in Fowler's syndrome – a specific NOUR entity, and patients with OAB. In NOUR, SNM may restore the periaqueductal gray activity through a diminution of excessive inhibitory afferent messages, particularly through modification of the activity of the median prefrontal cortex. Finally, sacral neuromodulation (SNM) may influence neural plasticity at the peripheral, spinal, and/or supraspinal levels; however, the underlying mechanisms and specific neurophysiological changes remain incompletely understood.</div></div><div><h3>Conclusion</h3><div>While our understanding of the mechanisms of action of SNM is still evolving, emerging data point toward a multifaceted process involving modulation of peripheral afferent input, spinal processing, and supraspinal structures - including those involved in sensorimotor integration, emotional regulation, and autonomic balance.</div></div>","PeriodicalId":55410,"journal":{"name":"Autonomic Neuroscience-Basic & Clinical","volume":"261 ","pages":"Article 103337"},"PeriodicalIF":3.3,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144893568","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Sacral nerve electrical stimulation (SNES) ameliorates bladder dysfunction and detrusor fibrosis in early-stage spinal cord injury: A randomized controlled experimental study in rats 骶神经电刺激(SNES)改善早期脊髓损伤大鼠膀胱功能障碍和逼尿肌纤维化:一项随机对照实验研究
IF 3.2 4区 医学 Q2 NEUROSCIENCES Pub Date : 2025-10-01 Epub Date: 2025-07-06 DOI: 10.1016/j.autneu.2025.103322
Lingyan Wang, Junhua Li, Chenhao Tang, Chen Song, Yanbin Wang
This study evaluated the therapeutic effects of sacral nerve electrical stimulation (SNES) targeting the L6-S1 spinal nerves on neurogenic bladder dysfunction following spinal cord injury (SCI). Using a randomized controlled design, 80 female Sprague-Dawley rats were divided into four groups: sham surgery, complete T9 spinal cord transection (SCI model), SCI with electrode implantation only (control), and SCI with active SNES (3–5 Hz, 3–5 V daily for 4 weeks). Bladder function was assessed through urodynamics, while detrusor fibrosis was examined using histological and ultrastructural analyses.
The SCI model group demonstrated significant urodynamic impairments compared to sham controls, including increased leak point pressure (43.15 ± 1.37 vs 25.52 ± 1.29 cmH2O) and decreased bladder capacity (1.52 ± 0.21 vs 4.21 ± 0.72 mL) and compliance (0.21 ± 0.14 vs 0.42 ± 0.26 mL/cmH2O; all P < 0.01). SNES treatment substantially reversed these abnormalities (P < 0.01 vs SCI group), restoring parameters to near-normal levels. Histological examination revealed that SNES significantly reduced collagen deposition (types I and III) in detrusor muscle compared to untreated SCI animals (P < 0.05). Transmission electron microscopy showed preserved mitochondrial structure in SNES-treated animals, contrasting with the cellular vacuolization observed in SCI controls.
These results demonstrate that early intervention with SNES at the L6-S1 level can effectively mitigate both functional and structural bladder impairments following SCI. The treatment improved urodynamic parameters while reducing fibrotic changes in detrusor muscle, suggesting its potential as a species-specific neuromodulation strategy for neurogenic bladder. This study provides experimental evidence supporting further investigation of sacral-level neuromodulation for SCI-related bladder dysfunction.
本研究评价了骶神经电刺激(SNES)对L6-S1脊神经损伤后神经源性膀胱功能障碍的治疗效果。采用随机对照设计,将80只雌性Sprague-Dawley大鼠分为4组:假手术组、完全T9脊髓横断组(SCI模型)、单纯电极植入组(对照组)和活动SNES组(3-5 Hz,每天3-5 V,持续4周)。通过尿动力学评估膀胱功能,通过组织学和超微结构分析检查逼尿肌纤维化。与假手术对照组相比,脊髓损伤模型组表现出明显的尿动力学损伤,包括泄漏点压力增加(43.15±1.37 vs 25.52±1.29 cmH2O),膀胱容量减少(1.52±0.21 vs 4.21±0.72 mL)和依从性(0.21±0.14 vs 0.42±0.26 mL/cmH2O);所有P <;0.01)。SNES治疗显著逆转了这些异常(P <;0.01 (SCI组),参数恢复到接近正常水平。组织学检查显示,与未治疗的SCI动物相比,SNES显著减少了逼尿肌胶原沉积(I型和III型)(P <;0.05)。透射电镜显示,与脊髓损伤对照组相比,snes治疗动物的线粒体结构保存完好。这些结果表明,早期干预L6-S1水平的SNES可以有效减轻脊髓损伤后的功能性和结构性膀胱损伤。该疗法改善了尿动力学参数,同时减少了逼尿肌的纤维化变化,这表明它有可能作为一种神经源性膀胱的物种特异性神经调节策略。本研究为进一步研究骶椎水平的神经调节对sci相关膀胱功能障碍的影响提供了实验证据。
{"title":"Sacral nerve electrical stimulation (SNES) ameliorates bladder dysfunction and detrusor fibrosis in early-stage spinal cord injury: A randomized controlled experimental study in rats","authors":"Lingyan Wang,&nbsp;Junhua Li,&nbsp;Chenhao Tang,&nbsp;Chen Song,&nbsp;Yanbin Wang","doi":"10.1016/j.autneu.2025.103322","DOIUrl":"10.1016/j.autneu.2025.103322","url":null,"abstract":"<div><div>This study evaluated the therapeutic effects of sacral nerve electrical stimulation (SNES) targeting the L6-S1 spinal nerves on neurogenic bladder dysfunction following spinal cord injury (SCI). Using a randomized controlled design, 80 female Sprague-Dawley rats were divided into four groups: sham surgery, complete T9 spinal cord transection (SCI model), SCI with electrode implantation only (control), and SCI with active SNES (3–5 Hz, 3–5 V daily for 4 weeks). Bladder function was assessed through urodynamics, while detrusor fibrosis was examined using histological and ultrastructural analyses.</div><div>The SCI model group demonstrated significant urodynamic impairments compared to sham controls, including increased leak point pressure (43.15 ± 1.37 vs 25.52 ± 1.29 cmH<sub>2</sub>O) and decreased bladder capacity (1.52 ± 0.21 vs 4.21 ± 0.72 mL) and compliance (0.21 ± 0.14 vs 0.42 ± 0.26 mL/cmH<sub>2</sub>O; all <em>P</em> &lt; 0.01). SNES treatment substantially reversed these abnormalities (P &lt; 0.01 vs SCI group), restoring parameters to near-normal levels. Histological examination revealed that SNES significantly reduced collagen deposition (types I and III) in detrusor muscle compared to untreated SCI animals (<em>P</em> &lt; 0.05). Transmission electron microscopy showed preserved mitochondrial structure in SNES-treated animals, contrasting with the cellular vacuolization observed in SCI controls.</div><div>These results demonstrate that early intervention with SNES at the L6-S1 level can effectively mitigate both functional and structural bladder impairments following SCI. The treatment improved urodynamic parameters while reducing fibrotic changes in detrusor muscle, suggesting its potential as a species-specific neuromodulation strategy for neurogenic bladder. This study provides experimental evidence supporting further investigation of sacral-level neuromodulation for SCI-related bladder dysfunction.</div></div>","PeriodicalId":55410,"journal":{"name":"Autonomic Neuroscience-Basic & Clinical","volume":"261 ","pages":"Article 103322"},"PeriodicalIF":3.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144580657","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Mechanisms underpinning peripheral chemoreceptor modulation of hypertension 外周化学受体调节高血压的机制
IF 3.2 4区 医学 Q2 NEUROSCIENCES Pub Date : 2025-10-01 Epub Date: 2025-06-23 DOI: 10.1016/j.autneu.2025.103317
Xin Shen, Julian F.R. Paton
On its activation, the carotid body (CB) provides one of the greatest stimulants to raise cardiovascular sympathetic activity. Through proof of principle studies the CB has been shown to be a major driver of the heightened sympathetic activity associated with several cardiometabolic diseases. Understanding the mechanisms of hypoxia and cellular transduction as well as inter-cellular signalling within the CB becomes crucial for identification of novel interventions to quench CB hyperactivity in disease. In this review, we summarise the mechanisms of hypoxia but also emphasise that the CB is more than an oxygen sensor which is acutely tuned to the regulation of both oxygen and glucose with feedback from blood-borne hormones regulating metabolism. This feature opens new druggable targets to restrain CB activity as well as the possibility to consider this organ as a nodal point for regulating autonomic dysfunction underpinning the metabolic syndrome.
在颈动脉体的激活过程中,颈动脉体为提高心血管交感神经活动提供了最大的刺激物之一。通过原理证明研究表明,脑后皮层是与几种心脏代谢疾病相关的交感神经活动增强的主要驱动因素。了解CB内缺氧和细胞转导以及细胞间信号传导的机制对于确定抑制疾病中CB过度活跃的新干预措施至关重要。在这篇综述中,我们总结了缺氧的机制,但也强调了CB不仅仅是一个氧传感器,它敏锐地调节氧气和葡萄糖,并从调节代谢的血源性激素反馈。这一特点开辟了新的药物靶点来抑制CB活性,并可能将该器官视为调节代谢综合征基础上的自主神经功能障碍的节点。
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引用次数: 0
Exercise and the autonomic nervous system: New insights and future directions 运动和自主神经系统:新的见解和未来的方向。
IF 3.3 4区 医学 Q2 NEUROSCIENCES Pub Date : 2025-10-01 Epub Date: 2025-07-16 DOI: 10.1016/j.autneu.2025.103333
James P. Fisher , Lauro C. Vianna
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引用次数: 0
Microneedle-assisted iontophoretic transdermal administration of adrenergic antagonists does not modulate palmar sweating induced by static exercise in healthy young adults 微针辅助离子透皮给药肾上腺素能拮抗剂不会调节健康年轻人静态运动引起的手掌出汗
IF 3.2 4区 医学 Q2 NEUROSCIENCES Pub Date : 2025-10-01 Epub Date: 2025-07-12 DOI: 10.1016/j.autneu.2025.103321
Hui Wang , Kaito Tamura , Shoma Oshima , Shotaro Yokoyama , Yumi Okamoto , Junto Otsuka , Hanano Kato , Hirofumi Yamashita , Ying-Shu Quan , Tatsuro Amano
Palmar sweating is primarily evoked by psychological and physical (e.g., exercise) stress, while the peripheral control of this response remains uncertain. We investigated whether the transdermal administration of adrenergic antagonists modulates palmar sweating induced by isometric knee extension (IKE) exercise. In a climate chamber (28 °C and 40 % relative humidity), 15 healthy young adult males completed IKE exercises at maximal (5 s maximum voluntary contraction, MVC) and submaximal (50 % MVC to exhaustion) effort, before and after the transdermal iontophoretic administration of bretylium (noradrenergic sympathetic nerve inhibitor), terazosin (α-adrenergic receptor antagonist), propranolol (β-adrenergic receptor antagonist), or NaCl (control) to the palm pretreated with solid microneedles to enhance skin permeability. The efficacy of terazosin and propranolol on the palm was assessed by administering α- and β-adrenergic agonists (phenylephrine and salbutamol combined with aminophylline, respectively) in follow-up studies, whereas bretylium efficacy was verified by evaluating cold-induced palmar cutaneous vasoconstriction. Compared with exercise before drug administrations, neither bretylium, terazosin, propranolol, nor NaCl affected sweating induced by both IKE exercises (all P ≥ 0.600, interaction and treatment effect). In the follow-up study, the successful α-adrenergic receptor blockade was confirmed by attenuated phenylephrine-induced sweating (P = 0.001). Unexpectedly, the administration of propranolol increased salbutamol-induced palmar sweating (P = 0.008), leaving the efficacy of β-adrenergic receptor blockade uncertain. The bretylium administration effectively abolished cold-induced cutaneous vasoconstriction (P = 0.006). In conclusion, this study demonstrates that transdermal administration of bretylium, terazosin, and propranolol does not alter palmar sweating induced by IKE exercise, implying the absence of adrenergic modulation.
手掌出汗主要是由心理和生理(如运动)压力引起的,而这种反应的外周控制仍然不确定。我们研究了肾上腺素能拮抗剂的经皮给药是否会调节等长膝关节伸展(IKE)运动引起的手掌出汗。在气候室(28°C和40%相对湿度)中,15名健康的年轻成年男性在经皮离子吸氧给药bretylium(去甲肾上腺素能交感神经抑制剂)、terazosin (α-肾上腺素能受体拮抗剂)、propranolol (β-肾上腺素能受体拮抗剂)之前和之后,以最大(5 s最大自愿收缩,MVC)和次最大(50% MVC至精疲力竭)的努力完成IKE运动。或NaCl(对照)到手掌,用固体微针预处理,以增强皮肤的渗透性。在后续研究中,泰拉唑嗪和心得安对手掌的疗效通过给予α-肾上腺素激动剂和β-肾上腺素激动剂(分别为苯肾上腺素和沙丁胺醇联合氨茶碱)来评估,而布雷特利姆的疗效通过评估冷诱导的手掌皮肤血管收缩来验证。与给药前运动相比,布雷利姆、特拉唑嗪、心得安、NaCl对两种IKE运动引起的出汗均无影响(P均≥0.600、相互作用及治疗效果)。在随访研究中,α-肾上腺素能受体阻断成功,苯肾上腺素引起的出汗减弱(P = 0.001)。出乎意料的是,普萘洛尔增加了沙丁胺醇引起的手掌出汗(P = 0.008),使β-肾上腺素能受体阻断的效果不确定。溴代溴铵能有效消除冷致皮肤血管收缩(P = 0.006)。总之,本研究表明,经皮给药布雷利姆、特拉唑嗪和心得安不会改变IKE运动引起的手掌出汗,这意味着不存在肾上腺素能调节。
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引用次数: 0
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Autonomic Neuroscience-Basic & Clinical
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