The Japanese journal of physiology最新文献

{"title":"Impaired ribosome biogenesis could contribute to anabolic resistance to strength exercise in the elderly","authors":"T. Chaillou","doi":"10.1113/JP273773","DOIUrl":"https://doi.org/10.1113/JP273773","url":null,"abstract":"Impaired ribosome biogenesis could contribute to anabolic resistance to strength exercise in the elderly","PeriodicalId":22512,"journal":{"name":"The Japanese journal of physiology","volume":"23 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74721223","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Post‐translational cleavage of Hv1 in human sperm tunes pH‐ and voltage‐dependent gating","authors":"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","doi":"10.1113/JP273189","DOIUrl":"https://doi.org/10.1113/JP273189","url":null,"abstract":"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.","PeriodicalId":22512,"journal":{"name":"The Japanese journal of physiology","volume":"64 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88925407","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Angiotensin II reduces the surface abundance of KV1.5 channels in arterial myocytes to stimulate vasoconstriction","authors":"Michael W. Kidd, Simon Bulley, J. Jaggar","doi":"10.1113/JP272893","DOIUrl":"https://doi.org/10.1113/JP272893","url":null,"abstract":"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.","PeriodicalId":22512,"journal":{"name":"The Japanese journal of physiology","volume":"28 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82325074","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Increasing pulmonary blood flow at birth: the nerve of the baby","authors":"Noah H. Hillman","doi":"10.1113/JP273783","DOIUrl":"https://doi.org/10.1113/JP273783","url":null,"abstract":"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","PeriodicalId":22512,"journal":{"name":"The Japanese journal of physiology","volume":"87 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89098187","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effect of α1‐adrenergic blockade on post‐exercise brachial artery flow‐mediated dilatation at sea level and high altitude","authors":"M. Tymko, J. Tremblay, Alex B. Hansen, C. Howe, C. Willie, M. Stembridge, D. Green, R. Hoiland, Prajan Subedi, J. Anholm, P. Ainslie","doi":"10.1113/JP273183","DOIUrl":"https://doi.org/10.1113/JP273183","url":null,"abstract":"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.","PeriodicalId":22512,"journal":{"name":"The Japanese journal of physiology","volume":"73 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79647910","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"All‐optical functional synaptic connectivity mapping in acute brain slices using the calcium integrator CaMPARI","authors":"Timothy A Zolnik, Fern Sha, F. W. Johenning, E. Schreiter, L. Looger, M. Larkum, R. Sachdev","doi":"10.1113/JP273116","DOIUrl":"https://doi.org/10.1113/JP273116","url":null,"abstract":"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.","PeriodicalId":22512,"journal":{"name":"The Japanese journal of physiology","volume":"29 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83279038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Breaking the cycle of intergenerational obesity.","authors":"Catherine E Aiken, Susan E Ozanne","doi":"10.1113/JP273821","DOIUrl":"10.1113/JP273821","url":null,"abstract":"","PeriodicalId":22512,"journal":{"name":"The Japanese journal of physiology","volume":"36 1","pages":"1443-1444"},"PeriodicalIF":0.0,"publicationDate":"2017-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5330879/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75770772","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurovascular mechanisms underlying augmented cold‐induced reflex cutaneous vasoconstriction in human hypertension","authors":"J. Greaney, W. Larry Kenney, L. Alexander","doi":"10.1113/JP273487","DOIUrl":"https://doi.org/10.1113/JP273487","url":null,"abstract":"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.","PeriodicalId":22512,"journal":{"name":"The Japanese journal of physiology","volume":"75 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83775153","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Parasympathetic withdrawal increases heart rate after 2 weeks at 3454 m altitude","authors":"C. Siebenmann, P. Rasmussen, Mike Hug, S. Keiser, D. Flück, J. Fisher, M. Hilty, M. Maggiorini, C. Lundby","doi":"10.1113/JP273726","DOIUrl":"https://doi.org/10.1113/JP273726","url":null,"abstract":"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.","PeriodicalId":22512,"journal":{"name":"The Japanese journal of physiology","volume":"71 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86131592","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sildenafil therapy for fetal cardiovascular dysfunction during hypoxic development: studies in the chick embryo.","authors":"Nozomi Itani, Katie L Skeffington, Christian Beck, Dino A Giussani","doi":"10.1113/JP273393","DOIUrl":"10.1113/JP273393","url":null,"abstract":"<p><strong>Key points: </strong>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.</p><p><strong>Abstract: </strong>There is a need for developing clinically translatable therapy for preventing fetal origins of cardiovascular disease in pregnancy complicated by chronic fetal hypoxia. Evidence shows that sildenafil protects placental perfusion and fetal growth. However, whether beneficial effects of sildenafil transcend onto the fetal heart and circulation in complicated development is unknown. We isolated the direct effects of sildenafil on the fetus using the chick embryo and hypothesised that sildenafil also protects fetal cardiovascular function in hypoxic development. Chick embryos (n = 11 per group) were incubated in normoxia or hypoxia (14% O₂ ) from day 1 and treated with sildenafil (4 mg kg^-1  day^-1 ) from day 13 of the 21-day incubation. Hypoxic incubation increased oxidative stress (4-hydroxynonenal, 141.1 ± 17.6% of normoxic control), reduced superoxide dismutase (60.7 ± 6.3%), increased phosphodiesterase type 5 expression (167 ± 13.7%) and decreased nitric oxide bioavailability (54.7 ± 6.1%) in the fetal heart, and promoted peripheral endothelial dysfunction (70.9 ± 5.6% AUC of normoxic control; all P < 0.05). Sildenafil treatment after onset of chronic hypoxia prevented the increase in phosphodiesterase expression (72.5 ± 22.4%), protected against oxidative stress (94.7 ± 6.2%) and normalised nitric oxide bioavailability (115.6 ± 22.3%) in the fetal heart, and restored endothelial function in the peripheral circulation (89.8 ± 2.9%). Sildenafil protects the fetal heart and circulation directly in hypoxic development via mechanisms including decreased oxidative stress and enhanced nitric oxide bioavailability. Sildenafil may be a good translational candidate for human antioxidant therapy to prevent fetal origins of cardiovascular dysfunction in adverse pregnancy.</p>","PeriodicalId":22512,"journal":{"name":"The Japanese journal of physiology","volume":"52 1","pages":"1563-1573"},"PeriodicalIF":0.0,"publicationDate":"2017-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5330925/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91283853","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}