bluuebunny/crossref_metadata_2025_split huggingface dataset:
Posture Modifies Neuro‐Cardiac Heart Rate Responses at the Onset of Moderate Intensity Isometric Handgrip Exercise
Authors: Woehrle Emilie , Jacobs Kaitlyn G. , Shoemaker J. Kevin 
Published: June 2021

BackgroundThe heart rate (HR) response at the onset of moderate intensity isometric handgrip (IHG) exercise is related to neural control of the heart, primarily vagal withdrawal. If so, modest modifications in neuro‐cardiac function by postural shifts should modify the HR response to exercise.ObjectiveThis study examined the effect of supine versus seated postures on the changes in HR and heart rate variability (HRV) at the onset of IHG.Methods13 healthy adults (24±3 years; 6 females) performed IHG at 35% and 50% of maximal voluntary contraction strength (MVC), each lasting 30 seconds and separated by at least one minute of rest. HR (electrocardiogram) and root mean square of successive differences (RMSSD) were recorded from the last 30 seconds of the 1 minute baseline prior to handgrip, and the last 10 seconds of each 30 second handgrip.ResultsBaseline HR increased from 68bpm to 76bpm (p<0.001; d=1) and RMSSD decreased from 56ms to 44ms (p=0.25; d=0.4) when shifting from supine to seated positions. Compared to the supine position, the ΔHR with 35% IHG decreased in the seated position (7bpm to 3bpm; p=0.01; d=0.71). Similarly, the ΔRMSSD with 35% IHG tended to be less in the seated versus supine positions (−31ms to −16ms; p=0.07; d=0.7). During 50% MVC work, the seated position exerted only a modest effect on the IHG‐induced ΔHR compared to supine (18bpm to 13bpm; p=0.06; d=0.47) whereas the ΔRMSSD from baseline to IHG was diminished in seated versus supine positions (−47ms to −22ms; p=0.001; d=0.78).ConclusionWith RMSSD as an indicator of changes in cardiovagal influence, these preliminary results indicate that small changes in posture modify parasympathetic modulation of HR responses at the onset of moderate‐intensity isometric handgrip.Support or Funding InformationSupported by the Natural Sciences and Engineering Research Council of Canada.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Blunted Blood Pressure to Hand Grip Exercise in Individuals with Intellectual Disabilities: Preliminary Results
Authors: Hilgenkamp Thessa , Schroeder Elizabeth C. , White Daniel W. , Baynard Tracy , Fernhall Bo 
Published: June 2021

Individuals with intellectual disabilities (ID) have limited work capacity. In individuals with Down syndrome, this has been previously linked to autonomic dysfunction. Previous research suggests autonomic dysfunction and altered hemodynamics may also be present in individuals with ID without Down syndrome but this has not been tested.PURPOSETo compare the autonomic and hemodynamic response to isometric handgrip (HG) exercise in individuals with ID to a control group without ID.METHODSNine individuals with ID and 19 individuals without ID had heart rate and blood pressure continuously recorded via an ECG‐lead and finger‐photoplethysmography in the seated position. Isometric HG was performed at 30% of maximal voluntary contraction for 2 min. Recordings were acquired for the last 2 min of quiet rest, HG, and the first 2 min of recovery.RESULTSIndividuals with ID showed smaller increases compared to individuals without ID for systolic and diastolic blood pressure, mean arterial pressure and pulse pressure during HG (p<0.001; Table).CONCLUSIONDespite no HRV differences, these preliminary results suggest a blunted blood pressure response to isometric HG in individuals with ID, which may help explain low fitness levels observed in this population.Support or Funding InformationThe research leading to these results has received funding from the People Programme (Marie Curie Actions) of the European Union's Seventh Framework Programme (FP7/2007–2013) under REA grant agreement no 625455.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
The Influence of Total Load on Cardiac Autonomic Recovery Following Resistance Exercise in Young and older adults
Authors: Sardeli Amanda Veiga , Fernandes Gáspari Arthur F. , Ferreira Marina Lívia Venturini , do Carmo Santos Lucas , Rosenberg Alexander J. , Fernhall Bo J. , Cavaglieri Cláudia Regina , Chacon‐Mikahil Mara Patrícia Traina 
Published: June 2021

IntroductionThe delay in cardiac autonomic recovery (CAR) following physical activity is associated with increased risk of cardiovascular events. Aging is a major risk factor for cardiovascular disease, and older adults have altered resting cardiac autonomic modulation than young individuals. The intensity of exercise also influences autonomic recovery in young individuals.ObjectiveTo compare the CAR following resistance exercise (RE) in young (Y) and older (O) men, using high and low intensity RE.MethodsThe two groups (Y: n=9, age=26.3±4y, BMI=22.3±1.5Kg/m2 and O: n=9, age=64.3±4y, BMI=26.2±1.8 Kg/m2) performed 4 sets of RE, using leg press equipment, until failure. Subjects performed two different protocols; RE at 80% of 1RM (RE80) and at 30% of 1RM (RE30) in a random sequence. Heart rate was measured via a heart rate monitor and CAR was obtained through heart rate variability analysis pre and 30‐min post‐RE. The change values for heart rate variability (post 30‐min – pre) were assessed by root mean square (RMSSD) of successive RR intervals (iRR), high and low frequency in normalized units (HF and LF, respectively) and analyzed by 2‐way ANOVA (group*load).ResultsThe table shows a greater reduction of iRR, RMSSD and HF and a greater increase of LF in Y compared to O. Since the total load was higher in Y compared to O in RE80 and RE30 (Y RE30: 13767 ± 4738 kg vs. O RE30: 7812 ± 2094 kg, p < 0.05, and Y RE80: 10921 ± 4201 kg vs. O RE80: 7488 ± 2040 kg, p < 0.05), we evaluated the change in heart rate variability as a function of TL. This correction eliminated differences between Y and O for iRR and RMSSD (p > 0.05), while HF and LF remained different between Y and O (p < 0.05).ConclusionY showed delayed CAR in protocols with both RE80 and RE30. The higher TL in Y did not explain the delayed CAR in this group, thus other factors are involved. It is possible the lower heart rate variability adjustments of O is associated with limiting increases in sympathetic and reductions in parasympathetic modulation during RE but this needs further investigation.Support or Funding InformationWe thanks the support of CNPq (Conselho Nacional de Desenvolvimento Científico e Tecnológico), FAEPEX (Fundo de Apoio ao Ensino, à Pesquisa e Extensão da Universidade Estadual de Campinas) and CAPES (Coordenação de Aperfeiçoamento de Pessoal de Nível Superior).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Rho Kinase and Na+/H+ Exchanger Mediate Endothelin‐1 Induced Pulmonary Arterial Smooth Muscle Cell Proliferation and Migration
Authors: Huetsch John Christian , Yun Xin , Jiang Haiyang , Shimoda Larissa 
Published: June 2021

ObjectiveRemodeling of the pulmonary vasculature, involving increased proliferation and migration of pulmonary arterial smooth muscle cells (PASMCs), is a key component of the pathology underlying pulmonary hypertension (PH). Endothelin‐1 (ET‐1) is known to be an important contributor to both pulmonary vasoconstriction and remodeling in PH. We aimed to determine whether ET‐1 modulates PASMC function via a pathway involving Rho kinase (ROCK) and the Na+/H+ exchanger (NHE).MethodsPASMCs were isolated from distal pulmonary arteries of male C57/B6 mice as well as male Wistar rats and expanded in culture. To measure NHE activity, cells were incubated with pH‐sensitive fluorescent dye and the Na+‐dependent recovery of intracellular pH (pHi) following acidification by ammonium pulse challenge was measured via fluorescence microscopy. NHE1 mRNA expression was measured via qRT‐PCR and protein expression was measured via immunoblot. Proliferation was assessed via ELISA for BrdU incorporation over 24 hr. Migration was measured over 24 hr using Transwell filters with 8 μm pores. Cells were treated with 10−8 M ET‐1 versus vehicle for 24–48 hr. NHE was pharmacologically inhibited with 10 μM ethyl‐isopropyl amiloride. ROCK was inhibited with 10 μM Y‐27632.ResultsET‐1 treatment, compared to vehicle, resulted in increased resting pHi and NHE activity in PASMCs. ET‐1 did not result in increased NHE1 mRNA or protein expression. ROCK inhibition prevented ET‐1‐induced NHE activation. PASMC proliferation and migration were both increased by ET‐1 treatment, compared to vehicle. ROCK inhibition attenuated PASMC proliferation and migration in the presence of ET‐1. Similarly, NHE inhibition also attenuated ET‐1‐induced PASMC proliferation and migration.ConclusionsET‐1 results in increased PASMC proliferation and migration via a pathway involving ROCK and NHE activation. This suggests a novel pathway which may contribute to vascular remodeling in PH.Support or Funding InformationNIH K08HL133475 & R01HL073859This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Involvement of medullary raphe on active expiration.
Authors: DO NASCIMENTO SILVA JOSIANE , dos Santos Moreira Thiago , Takakura Ana Carolina 
Published: June 2021

IntroductionIn rodents, the parafacial respiratory group (pFRG), located in the ventral lateral medulla, has been described as a conditional expiratory oscillator that emerges mainly in conditions of metabolic challenges to increase ventilation. However the mechanisms required to stimulate pFRG and generate active expiration have not been fully elucidated. Because the raphe region has long been described to be involved in breathing activity, we decided to investigate whether there were projections from raphe to pFRG and to analyze the effect of raphe inhibition on the active expiration generated by hypercapnia.ObjectiveInvestigate the possible involvement of the medullary raphe in active expiration mediated by hypercapnia.MethodsMale Wistar rats weighing 250–350g (CEUA: 80/13) were used. For anatomical experiments, animals received retrograde tracer FluorGold (FG) injections in the pFRG (n=4). Seven to ten days after the injections, immuhistochemistry for tryptophan hydroxylase (TrOH) was performed. For physiological experiments, urethane‐anesthetized rats received bilateral injection of the GABA‐A agonist muscimol (60 pmol/60 nl) in the Raphe Magnus (RMg) or Obscurus (ROb) regions, the electromyography of diaphragm (DiaEMG) and abdominal (AbdEMG) muscles were recorded.ResultsThe anatomical experiments showed that there were projections from serotonergic and non‐serotonergic neurons of RMg and ROb to pFRG region. The injection of muscimol in RMg or ROb did not significantly alter the frequency and amplitude of DiaEMG and did not generate active expiration. In these animals, hypercapnia after raphe inhibition did not produce significant changes on DiaEMG amplitude and frequency. However, inhibition of RMg or ROb produced an increase in the AbdEMG amplitude during hypercapnia.ConclusionOur results demonstrated that RMg and ROb project directly to pFRG and may be involved in active expiration. We propose that RMg and ROb may be modulating the activity of pFRG during hypercapnia.Support or Funding InformationFinancial support: FAPESP, CNPq and CAPESThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Hypercapnic ventilatory response (HcVR) is increased in a rat model of Alzheimer's disease
Authors: Vicente Mariane C. , Bicego Kenia C. , Carrettiero Daniel C. , Almeida Maria Camila , Gargaglioni Luciane H. 
Published: June 2021

Besides the typical cognitive decline, patients with Alzheimer's disease (AD) develop disorders in the respiratory system such as sleep apnea, shortness of breath and arrhythmias. These symptoms are aggravated with progression of the disease. However, the cause and nature of this disturbance are not well understood. Here, we, used an animal model for sporadic Alzheimer's disease (AD) induced by icv injection of streptozotocin (STZ) (2 mg/kg). We measured ventilation (VE) EEG and EMG during normocapnia, hypercapnia and hypoxia. In addition, we performed Western blot for phosphorylated Tau and β‐amyloid peptide (Aβ) in Locus Coeruleus (LC), Retrotrapezoid nucleus, Raphe Bulbar, Botzinger and Hippocampus and evaluated memory and learning acquisition by using the Barnes maze. STZ treatment promoted memory and learning deficits and an increase of 70% the of Aβ in the LC. STZ treated rats presented an increased HcVR during wakefulness (VE: STZ= 2456.7 ± 261.5 vs VE Vehicle= 1677.4 ±141.8 mL. Kg−1. min−1) and sleep (VE: STZ= (2106.9 ± 261.6 vs VE Vehicle= 1724.1 ± 37.4 mL. Kg−1. min−1). Our data suggest that sporadic AD animals present an increased sensitivity to CO2 possibly due an increased Aβ in the LC.Support or Funding InformationSão Paulo Research Foundation (FAPESP) and National Council for Scientific and Technological Development (CNPq)This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Laminin‐β6 integrin Interaction is Crucial for Coronary Collateral Growth
Authors: Joseph Gregory , D'Addario Catherine , McEvoy Kyle , Jadhav Rashmi , Hutcheson Brenda , Rocic Petra 
Published: June 2021

Extracellular matrix (ECM) composition and regulation is an essential component of coronary collateral growth (CCG). The ECM serves several functions which include mechanical and structural support, cell‐to‐cell communication, and regulation of cell mobility and phenotype. Laminin is a major component of the ECM. In the metabolic syndrome, the ECM composition is altered. In this study, we investigated the role of laminin and its binding to the β6 integrin in the regulation of CCG in response to repetitive ischemia (RI), and cellular processes involved in CCG. Coronary blood flow in Sprague‐Dawley (SD) or metabolic syndrome rats (JCR:LA‐cp, JCR), was measured in the collateral (CZ) and normal zone (NZ) of the heart using microspheres. Collateral‐dependent blood flow in JCR rats was impaired compared to SD rats (CZ/NZ flow ratio was 0.11±0.03 in JCR vs. 0.85±0.04 in SD), which correlated with decreased expression of laminin (~5 fold) and of the β6 integrin (~6 fold) in JCR animals. Administration of blocking‐antibodies against laminin or the β6 integrin in SD rats completely blocked CCG and decreased each other's expression, respectively. Furthermore, both laminin and β6 integrin expression were increased in endothelial cells (ECs) subjected to cycles of hypoxia‐hyperoxia‐normoxia to mimic RI vs. ECs cultured in normoxia. Blocking antibodies against laminin or the β6 integrin significantly impaired EC proliferation, migration and tube formation (~2–2.5 fold). TGF‐β signaling through Smad2/3 and leading to MMP 2/9 production, which is required for successful CCG, was also impaired (90%). Accordingly, TGF‐β receptor inhibition completely blocked CCG. Taken together, these results point to an important TGF‐β‐mediated pathway which promotes CCG and the activation of which is dependent on expression and the interaction between laminin and the β6 integrin.Support or Funding InformationSupport: NIH R01 HL093052This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Preconception Exposure of Particulate Matter Leads to Adult Cardiac Dysfunction through Altering Myocyte Function and Ca2+ Signaling Pathways
Authors: tanwar vineeta , Adelstein Jeremy , Sugar Benjamin , Schwieterman Neill , Youtz Dane , Falvo Michael , Wold Loren 
Published: June 2021

ObjectivePrevious studies have demonstrated that particulate matter, or ambient particles less than 2.5 μm (PM2.5) in diameter, exposure during both in utero and postnatal developmental periods triggers electrical remodeling and cardiac dysfunction during adulthood. This shows that PM2.5 can reprogram hearts during the gestational period. Despite this evidence, cardiac effects from pre‐gestational particulate matter exposure remain inconclusive. This study was performed to further investigate the potential priming effects of preconception exposure of PM2.5 on global cardiac dysfunction at adulthood.METHODSMale and female FVB mice were exposed separately to either filtered air (FA) or PM2.5 at a concentration (within the annual average range of 15 μg/m3 according to the National Ambient Air Quality Standards (NAAQS)) for 3 months. Mice were then cross bred into two groups: (1) FAm X FAf (both parents were FA exposed) and, (2) PMm X PMf (both parents were PM exposed). Offspring born to these crosses (PC FA and PC PM2.5) were analyzed at 3 months of age for in vivo cardiac function via echocardiography, followed by in vitro cardiomyocyte functional and molecular analyses.RESULTSEchocardiography identified increased LVESd (2.58 ± 0.13 PC FA, 2.93 ± 0.13 PC PM2.5, P=0.1) and reduced PWTs (1.70 ± 0.06 PC FA, 1.44 ± 0.08 PC PM2.5, P=0.05) dimensions in PC PM2.5‐exposed mice. Morphological alterations were associated with lower systolic function indicated by reduced fractional shortening % (35.09% ± 1.34 PC FA, 29.05% ± 1.25 PC PM2.5, P=0.03) and ejection fraction % (64.86% ± 1.76 PC FA, 56.27% ± 1.95 PC PM2.5, P=0.03) in PM2.5‐exposed mice. Cardiomyocytes isolated from PC PM2.5 mice showed reduced peak shortening %PS (12.93% ± 0.42 PC FA, 11.10% ± 0.41 PC PM2.5, P=0.002), −dL/dT (−10.60 ± 0.82 PC FA, −8.50 ± 0.60 PC PM2.5, P=0.05), TPS90 (0.08 ± 0.003 PC FA, 0.07 ± 0.002 PC PM2.5, P=0.05) and slower calcium reuptake (tau, 0.42±0.06 s FA, 0.67±0.09 s PC PM2.5, P=0.05). qPCR analyses revealed decreased MURC, MyBPC3 and increased Mypt1 expression and western blot analyses demonstrated modified NCX, SERCA and PLN expression in PC PM2.5‐exposed mice compared to PC FA‐exposed mice.CONCLUSIONSimilar to our previous study involving in utero exposure, preconception exposure to PC PM2.5 at real‐world concentrations results in adult cardiac dysfunction. These results suggest that abnormalities in developmental potential are not limited to prenatal or postnatal period but can also be determined prior to conception.Support or Funding InformationThis work is supported by funding from National Institutes of Health (RO1ES019923) to LEW.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Angiotensin‐II‐Induced Increase in Blood Pressure in Female and Male Mice
Authors: Rouch Al , Platt Anna , Fan Liming 
Published: June 2021

The kidney regulates blood pressure by controlling urinary salt and water excretion. Angiotensin II (AngII), a key player in controlling blood pressure, constricts blood vessels, stimulates vasopressin and aldosterone release, stimulates thirst, and increases sodium absorption from the proximal tubule. All effects cause increased blood pressure. Sex differences in the regulation of arterial blood pressure involve events surrounding the renin‐angiotensin‐aldosterone system. Evidence generally supports a protective mechanism for females with AngII‐induced hypertension; although, conflicting evidence exists. The purpose of this study was to investigate sex differences in CD‐1 mice under AngII administration for a period of 10 days. We hypothesized that female mice would be protected from AngII‐induced increase in mean arterial pressure (MAP) compared to male mice and that the renal handling of salt and water contributes to this protection. Four‐week old CD‐1 mice were obtained from Envigo, Inc. (Indianapolis, IN). Two studies, one with females and one with males, were conducted. Mice were placed in metabolic cages and consumed normal diet and water, ad libitum, for 15 days. After the first 5 days, an Alzet™ minipump containing either AngII (n=5) or vehicle (n=5) was implanted subcutaneously in each mouse to ensure continuous AngII infusion (1 mg/kg/min). Daily measurements included MAP via the tail‐cuff method (Kent Scientific, CODA System), urinary output, and urinary sodium excretion. MAP (mmHg) was not different between females and males in the 5‐day control period (85.1 ± 3.7 vs 81.7 ± 4.0, respectively). AngII‐treatment increased MAP in both females and males (110.3 ± 4.4 and 105.8 ± 3.0, p<0.001, compared to respective control period). Interestingly, AngII‐treated females showed higher urine output than AngII‐treated males (9.7 ± 0.8 vs 7.4 ± 0.4 ml/day, p<0.05) and also had higher sodium excretion (242 mEq/day vs 166 mEq/day, p<0.01). Absolute food intake in females and males was not different, however, females consumed more food per body weight. We conclude that female mice are not protected from AngII‐induced increase in MAP compared to male mice for a 10‐day AngII infusion period. However, based on the sodium excretion data, protection may be observed later from increased urine and sodium output in females. Results suggest that the renal handling of salt and water could be an important determinant of sex differences in blood pressure regulation.Support or Funding InformationNational Institute of General Medical Sciences of National Institutes of Health through Grant Number 8P20GM103447This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.