The Japanese journal of physiology最新文献

英文中文

Impaired ribosome biogenesis could contribute to anabolic resistance to strength exercise in the elderly 受损的核糖体生物发生可能有助于老年人对力量运动的合成代谢抵抗

The Japanese journal of physiology

Pub Date : 2017-03-01 DOI: 10.1113/JP273773

T. Chaillou

Impaired ribosome biogenesis could contribute to anabolic resistance to strength exercise in the elderly

受损的核糖体生物发生可能有助于老年人对力量运动的合成代谢抵抗

引用次数: 7

Post‐translational cleavage of Hv1 in human sperm tunes pH‐ and voltage‐dependent gating 人类精子中Hv1的翻译后裂解调节pH和电压依赖性门控

The Japanese journal of physiology

Pub Date : 2017-03-01 DOI: 10.1113/JP273189

Thomas K Berger, David M. Fußhöller, Normann Goodwin, W. Bönigk, A. Müller, Nasim Dokani Khesroshahi, C. Brenker, D. Wachten, E. Krause, U. Kaupp, T. Strünker

In human sperm, proton flux across the membrane is controlled by the voltage‐gated proton channel Hv1. We show that sperm harbour both Hv1 and an N‐terminally cleaved isoform termed Hv1Sper. The pH‐control of Hv1Sper and Hv1 is distinctively different. Hv1Sper and Hv1 can form heterodimers that combine features of both constituents. Cleavage and heterodimerization of Hv1 might represent an adaptation to the specific requirements of pH control in sperm.

在人类精子中，质子通过膜的通量是由电压门控质子通道Hv1控制的。我们发现精子同时含有Hv1和一种被称为Hv1Sper的N端分裂异构体。Hv1Sper和Hv1的pH控制明显不同。Hv1Sper和Hv1可以形成结合两种成分特征的异源二聚体。Hv1的分裂和异源二聚化可能代表了对精子pH控制的特殊要求的适应。

引用次数: 43

Angiotensin II reduces the surface abundance of KV1.5 channels in arterial myocytes to stimulate vasoconstriction 血管紧张素II降低了动脉肌细胞中KV1.5通道的表面丰度，从而刺激血管收缩

The Japanese journal of physiology

Pub Date : 2017-03-01 DOI: 10.1113/JP272893

Michael W. Kidd, Simon Bulley, J. Jaggar

Several different voltage‐dependent K+ (KV) channel isoforms are expressed in arterial smooth muscle cells (myocytes). Vasoconstrictors inhibit KV currents, but the isoform selectivity and mechanisms involved are unclear. We show that angiotensin II (Ang II), a vasoconstrictor, stimulates degradation of KV1.5, but not KV2.1, channels through a protein kinase C‐ and lysosome‐dependent mechanism, reducing abundance at the surface of mesenteric artery myocytes. The Ang II‐induced decrease in cell surface KV1.5 channels reduces whole‐cell KV1.5 currents and attenuates KV1.5 function in pressurized arteries. We describe a mechanism by which Ang II stimulates protein kinase C‐dependent KV1.5 channel degradation, reducing the abundance of functional channels at the myocyte surface.

几种不同的电压依赖性K+ (KV)通道亚型在动脉平滑肌细胞(肌细胞)中表达。血管收缩剂抑制KV电流，但其亚型选择性和机制尚不清楚。我们发现血管紧张素II (Ang II)，一种血管收缩剂，刺激KV1.5的降解，而不是KV2.1，通过蛋白激酶C和溶酶体依赖机制，减少了肠系膜动脉肌细胞表面的丰度。angii诱导的细胞表面KV1.5通道的减少降低了整个细胞的KV1.5电流，并减弱了加压动脉中的KV1.5功能。我们描述了Ang II刺激蛋白激酶C依赖性KV1.5通道降解的机制，减少了肌细胞表面功能通道的丰度。

引用次数: 13

Increasing pulmonary blood flow at birth: the nerve of the baby 出生时肺血流量增加:婴儿的神经

The Japanese journal of physiology

Pub Date : 2017-03-01 DOI: 10.1113/JP273783

Noah H. Hillman

The transition from a fetus to a newborn infant is one of the most dramatic and important physiological changes in an individual’s life. With the cutting of the umbilical cord, the fetus must almost instantly convert to newborn physiology, which relies on efficient gas exchange in the lungs, energy metabolism in the liver, and thermoregulation through brown fat (Hillman et al. 2012). The most crucial of these physiological shifts at birth is the transition from the fetal circulator pattern to normal dual ventricular physiology (Hooper et al. 2015). In utero, the pulmonary vascular resistance (PVR) is high and the majority (80–90%) of the blood return from the placenta is shunted through the foramen ovale and ductus arteriosus into the systemic circulation. With minimal blood return from the pulmonary vasculature, the left ventricular preload is highly dependent on the atrial shunt. With removal of the placenta at birth, the systemic vascular resistance rapidly increases, leading to increased left atrial pressures and closure of the foramen ovale. The pulmonary blood flow must simultaneously increase, through a decrease in PVR, to provide adequate preload to the left ventricle. Failure to decrease PVR leads to decreased cardiac output and the hypertension seen in the newborn condition – persistent pulmonary hypertension of the newborn. Closure of the ductus arteriosus completes the transition to newborn. The majority of normal newborns have rapid decreases of PVR in the first minutes after birth with recruitment of the lung, but up to 10% of infants will require some assistance at birth with the conversion to a newborn physiology. Aeration of the lung is essential for clearing the airways of fetal lung fluid and increasing pulmonary blood flow (Hillman et al. 2012). Infants generate large, negative pressure breaths at birth to force the fluid out of the airways and allow for gas exchange. By using a unique phase-contrast X-ray system on slightly preterm rabbit pups (kittens), Hooper et al. have studied the lung recruitment at birth (Hooper et al. 2007, 2016). They demonstrated that fetal lung fluid is cleared into the interstitial space only during inspiration. The use of positive end-expiratory pressure during ventilation at birth improves the uniformity of lung recruitment and decreases the back-flow of interstitial fluid into airways during exhalation (Hooper et al. 2016). Simultaneous decrease in PVR occurs with airway clearance. The aeration of the alveoli increases transmural pressures on the capillaries to increase capillary diameter and increase pulmonary blood flow (PBF) (Hooper et al. 2016). Pulmonary stretch also causes prostacyclin (PGI2) release from vascular endothelial cells to relax arterial smooth muscle. Increased oxygen tension after birth increases nitric oxide production in the endothelial cells to relax vessels. With the addition of iodine angiography to the phase contrast X-ray rabbit model, Lang and colleagues have been abl

从胎儿到新生儿的转变是一个人一生中最引人注目和最重要的生理变化之一。随着脐带的切断，胎儿必须几乎立即转变为新生儿的生理状态，这依赖于肺部有效的气体交换、肝脏的能量代谢和棕色脂肪的体温调节(Hillman et al. 2012)。出生时这些生理转变中最关键的是从胎儿循环系统模式到正常双心室生理的转变(Hooper etal . 2015)。在子宫内，肺血管阻力(PVR)很高，大部分(80-90%)从胎盘返回的血液通过卵圆孔和动脉导管分流进入体循环。由于肺血管回血最少，左心室预负荷高度依赖于心房分流。随着出生时胎盘的移除，全身血管阻力迅速增加，导致左心房压力增加和卵圆孔关闭。肺动脉血流量必须同时增加，通过PVR的降低，为左心室提供足够的预负荷。未能降低PVR导致心排血量减少和新生儿高血压——新生儿持续性肺动脉高压。动脉导管闭合完成向新生儿的过渡。大多数正常新生儿在出生后的最初几分钟内，随着肺的恢复，PVR迅速下降，但高达10%的婴儿在出生时需要一些帮助才能转化为新生儿生理。肺通气对于清除胎儿肺液气道和增加肺血流量至关重要(Hillman etal . 2012)。婴儿在出生时产生巨大的负压呼吸，以迫使液体排出气道并允许气体交换。Hooper等人通过使用一种独特的相衬x射线系统对轻微早产的兔幼崽(小猫)进行了出生时肺部补充的研究(Hooper et al. 2007, 2016)。他们证明，只有在吸气时，胎儿肺液才被清除到肺间质。出生时通气时使用呼气末正压可改善肺复吸的均匀性，并减少呼气时间质液回流到气道(Hooper et al. 2016)。PVR的同时降低发生在气道清除率。肺泡通气会增加毛细血管的跨壁压力，从而增加毛细血管直径，增加肺血流量(PBF) (Hooper et al. 2016)。肺动脉伸展也引起血管内皮细胞释放前列环素(PGI2)，使动脉平滑肌松弛。出生后增加的氧张力增加了内皮细胞中一氧化氮的产生，使血管放松。通过在兔x线相衬模型中加入碘血管造影，Lang和他的同事已经能够同时评估气道招募和肺血流。他们之前证明，用100%氮气对一个肺进行单侧通气，会增加充气肺和未通气肺的肺血流量(Lang et al. 2016)。与氮气或空气相比，100%氧气通气增加了双肺的扩张作用。Lang et al.(2017)在本期的The Journal of Physiology上进一步探讨了迷走神经刺激对出生时肺血流量增加的作用。在开始通气之前，通过迷走神经进行双侧切开或假手术。在呼吸管闭塞的情况下，小猫被分配到100%氮气、空气或100%氧气的单肺通气。通气2min后(全程x线及血管造影)，由单肺通气转为双肺通气。Lang等人(2017)证实了先前的研究结果，即出生时单肺充气100%氮的对侧肺血流量增加，并证明这种增加在迷走神经切除术的小猫中被阻断。迷走神经切开术也降低了通常在通气时发现的心率增加。初次呼吸时使用氧气会引起肺两侧血管扩张，而不切断迷走神经。作者认为，胎儿肺液从气道中清除后，肺间质组织内压力的增加刺激了迷走神经的c纤维。氧的加性效应证实，存在多重重叠刺激，以确保PVR发生临界下降。迷走神经反应的存在对早产儿尤其重要，早产儿由于表面活性剂缺乏而出现不均匀的肺扩张，需要快速增加通过双肺的肺血流量来维持心输出量。这项研究支持了新生儿复苏指南在进行更高级的心肺复苏之前建立适当通气的重要性。了解出生时的生理转变对制定新生儿复苏指南至关重要。在PVR下降和PBF增加之前，在出生时立即剪断脐带，会导致左心室预负荷迅速下降和全身血压发生变化(Hooper et al. 2015)。左心室输出量减少导致脑血流改变，这可能影响极早产儿的脑室内出血。在早产儿羊中，在移除胎盘之前进行通气可以维持脑血流量，并且最近已经开始招募人类研究(Hooper et al. 2015)。目前的研究强调了肺通气的重要性，部分通过迷走神经刺激，在出生时PVR的关键下降需要一个人的生命中最戏剧性的转变。

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引用次数: 2

The effect of α1‐adrenergic blockade on post‐exercise brachial artery flow‐mediated dilatation at sea level and high altitude α - 1 -肾上腺素能阻断对运动后肱动脉血流介导的扩张的影响

The Japanese journal of physiology

Pub Date : 2017-03-01 DOI: 10.1113/JP273183

M. Tymko, J. Tremblay, Alex B. Hansen, C. Howe, C. Willie, M. Stembridge, D. Green, R. Hoiland, Prajan Subedi, J. Anholm, P. Ainslie

Our objective was to quantify endothelial function (via brachial artery flow‐mediated dilatation) at sea level (344 m) and high altitude (3800 m) at rest and following both maximal exercise and 30 min of moderate‐intensity cycling exercise with and without administration of an α1‐adrenergic blockade. Brachial endothelial function did not differ between sea level and high altitude at rest, nor following maximal exercise. At sea level, endothelial function decreased following 30 min of moderate‐intensity exercise, and this decrease was abolished with α1‐adrenergic blockade. At high altitude, endothelial function did not decrease immediately after 30 min of moderate‐intensity exercise, and administration of α1‐adrenergic blockade resulted in an increase in flow‐mediated dilatation. Our data indicate that post‐exercise endothelial function is modified at high altitude (i.e. prolonged hypoxaemia). The current study helps to elucidate the physiological mechanisms associated with high‐altitude acclimatization, and provides insight into the relationship between sympathetic nervous activity and vascular endothelial function.

我们的目的是量化在海平面(344米)和高海拔(3800米)休息时的内皮功能(通过肱动脉血流介导的扩张)，以及在最大运动和30分钟的中等强度自行车运动(有α1 -肾上腺素能阻断剂和无α1 -肾上腺素能阻断剂)后。在休息时，臂内皮功能在海平面和高海拔之间没有差异，在最大运动后也没有差异。在海平面上，中等强度运动30分钟后，内皮功能下降，α1 -肾上腺素能阻断可消除这种下降。在高海拔地区，中等强度运动30分钟后，内皮功能不会立即下降，α1 -肾上腺素能阻滞导致血流介导的扩张增加。我们的数据表明，运动后内皮功能在高海拔地区发生改变(即长时间的低氧血症)。本研究有助于阐明高原适应的相关生理机制，并为交感神经活动与血管内皮功能之间的关系提供见解。

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引用次数: 18

All‐optical functional synaptic connectivity mapping in acute brain slices using the calcium integrator CaMPARI 利用钙整合子CaMPARI在急性脑切片中绘制全光学功能突触连接图谱

The Japanese journal of physiology

Pub Date : 2017-03-01 DOI: 10.1113/JP273116

Timothy A Zolnik, Fern Sha, F. W. Johenning, E. Schreiter, L. Looger, M. Larkum, R. Sachdev

The genetically encoded fluorescent calcium integrator calcium‐modulated photoactivatable ratiobetric integrator (CaMPARI) reports calcium influx induced by synaptic and neural activity. Its fluorescence is converted from green to red in the presence of violet light and calcium. The rate of conversion – the sensitivity to activity – is tunable and depends on the intensity of violet light. Synaptic activity and action potentials can independently initiate significant CaMPARI conversion. The level of conversion by subthreshold synaptic inputs is correlated to the strength of input, enabling optical readout of relative synaptic strength. When combined with optogenetic activation of defined presynaptic neurons, CaMPARI provides an all‐optical method to map synaptic connectivity.

基因编码的荧光钙积分器钙调制光激活比率积分器(CaMPARI)报告了由突触和神经活动诱导的钙内流。它的荧光在紫光和钙的作用下由绿色变为红色。转化率——对活性的敏感度——是可调的，取决于紫光的强度。突触活性和动作电位可以独立启动显著的CaMPARI转换。阈下突触输入的转换水平与输入的强度相关，从而实现相对突触强度的光学读出。当CaMPARI结合光遗传学激活定义的突触前神经元时，CaMPARI提供了一种全光学方法来绘制突触连接。

引用次数: 27

Breaking the cycle of intergenerational obesity 打破代际肥胖的循环

The Japanese journal of physiology

Pub Date : 2017-03-01 DOI: 10.1113/JP273821

C. Aiken, S. Ozanne

Abstract There is now a large body of evidence describing the significant risk of obesity and metabolic complications in the children of mothers who were over-weight or obese during. This article is protected by copyright. All rights reserved

引用次数: 2

Sildenafil therapy for fetal cardiovascular dysfunction during hypoxic development: studies in the chick embryo 西地那非治疗缺氧发育期间胎儿心血管功能障碍:在鸡胚胎中的研究

The Japanese journal of physiology

Pub Date : 2017-03-01 DOI: 10.1113/JP273393

N. Itani, K. Skeffington, C. Beck, D. Giussani

Common complications of pregnancy, such as chronic fetal hypoxia, trigger a fetal origin of cardiovascular dysfunction and programme cardiovascular disease in later life. Sildenafil treatment protects placental perfusion and fetal growth, but whether the effects of sildenafil transcend the placenta to affect the fetus is unknown. Using the chick embryo model, here we show that sildenafil treatment directly protects the fetal cardiovascular system in hypoxic development, and that the mechanisms of sildenafil protection include reduced oxidative stress and increased nitric oxide bioavailability; Sildenafil does not protect against fetal growth restriction in the chick embryo, supporting the idea that the protective effect of sildenafil on fetal growth reported in mammalian studies, including humans, is secondary to improved placental perfusion. Therefore, sildenafil may be a good candidate for human translational antioxidant therapy to protect the chronically hypoxic fetus in adverse pregnancy.

常见的妊娠并发症，如慢性胎儿缺氧，可触发胎儿起源的心血管功能障碍，并在以后的生活中规划心血管疾病。西地那非治疗可保护胎盘灌注和胎儿生长，但西地那非的作用是否超越胎盘影响胎儿尚不清楚。通过鸡胚模型，我们发现西地那非直接保护缺氧发育中的胎儿心血管系统，其保护机制包括降低氧化应激和增加一氧化氮的生物利用度;在鸡胚中，西地那非不能防止胎儿生长受限，这支持了在哺乳动物(包括人类)研究中报道的西地那非对胎儿生长的保护作用是继发于改善胎盘灌注的观点。因此，西地那非可能是人类翻译抗氧化治疗的一个很好的候选者，以保护不良妊娠中的慢性缺氧胎儿。

引用次数: 27

Neurovascular mechanisms underlying augmented cold‐induced reflex cutaneous vasoconstriction in human hypertension 人类高血压中增强冷诱导反射性皮肤血管收缩的神经血管机制

The Japanese journal of physiology

Pub Date : 2017-03-01 DOI: 10.1113/JP273487

J. Greaney, W. Larry Kenney, L. Alexander

In hypertensive adults (HTN), cardiovascular risk increases disproportionately during environmental cold exposure. Despite ample evidence of dysregulated sympathetic control of the peripheral vasculature in hypertension, no studies have examined integrated neurovascular function during cold stress in HTN. The findings of the present study show that whole‐body cold stress elicits greater increases in sympathetic outflow directed to the cutaneous vasculature and, correspondingly, greater reductions in skin blood flow in HTN. We further demonstrate an important role for non‐adrenergic sympathetic co‐transmitters in mediating the vasoconstrictor response to cold stress in hypertension. In the context of thermoregulation and the maintenance of core temperature, sympathetically‐mediated control of the cutaneous vasculature is not only preserved, but also exaggerated in hypertension. Given the increasing prevalence of hypertension, clarifying the mechanistic underpinnings of hypertension‐induced alterations in neurovascular function during cold exposure is clinically relevant.

在高血压成人(HTN)中，在环境寒冷暴露期间，心血管风险不成比例地增加。尽管有大量证据表明高血压患者周围血管的交感神经控制失调，但尚未有研究检查HTN患者冷应激时的综合神经血管功能。本研究的结果表明，全身冷应激引起指向皮肤脉管系统的交感神经流出量的增加，相应地，HTN中皮肤血流量的减少。我们进一步证明了非肾上腺素能交感神经递质在高血压患者冷应激时介导血管收缩反应中的重要作用。在体温调节和核心温度维持的背景下，交感神经介导的对皮肤血管系统的控制在高血压中不仅被保留，而且被夸大。鉴于高血压患病率的增加，阐明寒冷暴露期间高血压诱导的神经血管功能改变的机制基础具有临床意义。

引用次数: 24

Parasympathetic withdrawal increases heart rate after 2 weeks at 3454 m altitude 在海拔3454米2周后，副交感神经戒断增加心率

The Japanese journal of physiology

Pub Date : 2017-03-01 DOI: 10.1113/JP273726

C. Siebenmann, P. Rasmussen, Mike Hug, S. Keiser, D. Flück, J. Fisher, M. Hilty, M. Maggiorini, C. Lundby

Heart rate is increased in chronic hypoxia and we tested whether this is the result of increased sympathetic nervous activity, reduced parasympathetic nervous activity, or a non‐autonomic mechanism. In seven lowlanders, heart rate was measured at sea level and after 2 weeks at high altitude after individual and combined pharmacological inhibition of sympathetic and/or parasympathetic control of the heart. Inhibition of parasympathetic control of the heart alone or in combination with inhibition of sympathetic control abolished the high altitude‐induced increase in heart rate. Inhibition of sympathetic control of the heart alone did not prevent the high altitude‐induced increase in heart rate. These results indicate that a reduced parasympathetic nervous activity is the main mechanism underlying the elevated heart rate in chronic hypoxia.

心率在慢性缺氧时增加，我们测试了这是交感神经活动增加、副交感神经活动减少还是非自主机制的结果。在7名低地居民中，在单独或联合药物抑制交感和/或副交感神经控制心脏后，在海平面和高海拔2周后测量心率。单独抑制副交感神经控制或联合抑制交感神经控制可消除高海拔引起的心率增加。单独抑制交感神经对心脏的控制并不能阻止高海拔引起的心率增加。这些结果表明，副交感神经活动减少是慢性缺氧时心率升高的主要机制。

引用次数: 20

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