bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cerebrovascular Reactivity in Resistance Trained Young Men
Authors: Corkery Adam T. , Miller Kathleen B. , Howery Anna J. , Barnes Jill N. 
Published: June 2021

Cerebrovascular reactivity is a measure of cerebrovascular function and is often used as an indicator of cerebrovascular health. There is evidence that habitual exercise can influence cerebrovascular reactivity; however, the effect of habitual exercise has only been examined in aerobic trained individuals or under the context of cardiorespiratory fitness. Therefore, the purpose of our study was to investigate the effect of chronic resistance training on cerebrovascular reactivity. We recruited 22 young men, including 11 untrained (UT; age = 27 ± 4 yr) and 11 resistance trained (RT; age = 24 ± 4 yr) individuals. Middle cerebral artery velocity (MCAv), beat‐to‐beat mean arterial blood pressure (MAP), and end‐tidal CO2 (ETCO2) were continuously monitored during a stepped hypercapnia protocol. In order to account for the influence of blood pressure on MCAv, cerebrovascular conductance index (CVCi) was calculated as MCAv/MAP × 100. MCAv, MAP, and CVCi reactivities were calculated as the linear relationship between each respective variable and ETCO2. There were no group differences in MCAv, MAP, CVCi, or ETCO2 during baseline or any level of the stepped hypercapnia (p > 0.05 for all). There was a trend for RT adults to have a higher MCAv reactivity, compared to UT adults (RT: 2.4 ± 0.4 cm/s/mmHg vs. UT: 1.7 ± 0.2 cm/s/mmHg; p = 0.06); however, there were no group differences in CVCi reactivity (RT: 1.5 ± 0.6 cm/s/mmHg2 vs. UT: 1.6 ± 0.2 cm/s/mmHg2; p = 0.41). Additionally, the MAP response to hypercapnia differed between the groups, as RT adults had a greater MAP reactivity compared with UT adults (RT: 0.98 ± 0.40 mmHg/mmHg vs. UT: 0.25 ± 0.08 mmHg/mmHg; p < 0.05). In conclusion, chronic resistance training likely influences cerebrovascular reactivity, as RT individuals had a larger MAP reactivity and a trend for greater MCAv reactivity, compared with UT individuals. Our results suggest that in young men, chronic resistance training may influence the hemodynamic response to a physiological stimulus, such as hypercapnia.Support or Funding InformationSupported by National Institute of Health grant HL118154This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Similar dysfunctional Ca2+ regulation in coronary smooth muscle from explanted human hearts and Ossabaw miniature swine strongly supports the translational relevance of this large animal model
Authors: Badin Jill K. , Eggenberger Caleb , Rodenbeck Stacey Dineen , Alloosh Mouhamad , Hashmi Zubair A. , Wang I‐wen , Sturek Michael 
Published: June 2021

IntroductionEstablishing a suitable animal model for metabolic syndrome (MetS) and coronary artery disease (CAD) is a challenge, as there are numerous risk factors and uncontrollable variables in the human population. However, Ossabaw miniature swine have been used with great success to recapitulate MetS and CAD in. The goal of this study was to determine whether the Ossabaw miniature swine is a clinically relevant large animal model on the cellular level, specifically with regards to intracellular Ca2+ ([Ca2+]i) handling, which is crucial for coronary smooth muscle (CSM) function.MethodsExplanted human hearts from 32 heart failure patients (22 male, 10 female; aged 53.4 ± 2.1 years) undergoing transplantation surgery at the Methodist Hospital in Indianapolis, IN were collected. Coronary arteries were excised and CSM cells were enzymatically dispersed and loaded with the fluorescent [Ca2+]i indicator fura‐2. [Ca2+]i levels were measured during depolarization‐induced Ca2+ influx and caffeine‐induced sarcoplasmic reticulum (SR) Ca2+ store release.ResultsIn explanted human hearts exhibiting either ischemic or dilated non‐ischemic cardiomyopathy, a greater coronary artery neointima formation was inversely correlated to depolarization‐induced Ca2+ influx and SR Ca2+ release in CSM cells. Furthermore, a greater number of MetS risk factors, including some factors individually (body mass index, LDL/HDL cholesterol ratio) was also correlated to decreased Ca2+ entry and, in patients with ischemic cardiomyopathy, decreased SR Ca2+ store release. Increased age, however, was correlated to an increased SR Ca2+ store release. These data are all consistent with previous studies of Ossabaw swine CSM.ConclusionThe similar CSM Ca2+ regulation in coronary arteries of humans and Ossabaw swine provides strong evidence for the phenomenal translational relevance of this large animal model, both on the whole‐animal level and the CSM [Ca2+]i signaling level.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Differential Renal and Lumbar Sympathetic Nerve Activation Following Myocardial Infarction in Rats
Authors: Yoshimoto Misa , Ikegame Shizuka , Hyodo Fumi , Shiwa Yuki , Miki Kenju 
Published: June 2021

Sympathetic nerve activation is considered an important contributor to mortality following acute myocardial infarction (MI). However, few studies have directly monitored sympathetic nerve activity (SNA) in response to acute MI. Herein, we directly and continuously monitored renal SNA (RSNA) and lumbar SNA (LSNA) before and after MI induced by left anterior descending artery (LAD) ligation. Wistar rats were instrumented with a telemetry transmitter and bipolar electrodes for continuous measurement of mean arterial pressure (MAP), heart rate (HR), RSNA, and LSNA. At 7 days after initial surgery, MAP, HR, RSNA, and LSNA were monitored continuously for 28 days. After 4 days of baseline measurements, rats received either LAD ligation via left thoracotomy (MI group; n=13) or sham surgery (n=11) under inhalation anesthesia. Rats in the MI group were subdivided into those that survived for 24 days (MI‐survivor group) and those that died within 3 days (MI‐3d group) after LAD ligation. Transthoracic echocardiography was performed before and aftJSOn day 1 in the MI‐3d group, LSNA increased by 202% ± 28% and MAP decreased by 38±4 mmHg compared with baseline values, while there were no changes in RSNA and HR. On day 1 in the MI‐survivor group, LSNA showed a trend towards an increase compared with baseline values, while there were no changes in RSNA and HR. In the MI‐survivor group, RSNA increased gradually from day 9, and peaked at day 24 (27%±14%) compared with the sham group, while there were no significant changes in MAP, HR, or LSNA. These data suggest that the RSNA may play an important role in compensating for impaired cardiac performance caused by MI, and that the LSNA and RSNA respond differently and in a region‐specific manner to MI.Support or Funding InformationJSPS Grant.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
The association of family history of hypertension and overweight induced early impairment in markers of oxidative stress and in heart rate variability
Authors: Viana Ariane , da Silva Dias Danielle , Nascimento Mario Cesar , dos Santos Fernando , Consolim‐Colombo Fernanda Marciano , Irigoyen Maria Cláudia , De Angelis Kátia 
Published: June 2021

Considering the high prevalence of hypertension worldwide and the changes in lifestyle, the understanding of the mechanisms involved in the genesis of hypertension are important to reach more precise interventions. Our objective was to evaluate cardiovascular, autonomic and oxidative stress parameters in individuals with family history of hypertension (FH) with or without overweight. We performed a cross‐sectional study and selected 65 healthy sedentary men (24.08 ± 5.84 years) distributed into 4 groups: negative FH eutrophic (FNE, n=18) or with overweight (FNO, n=19) and positive FH eutrophic (FHE, n=17) or with overweight (FHO, n=17). The heart rate variability (HRV) was analyzed at rest by spectral analysis. The oxidative stress markers were evaluated in plasma. A positive correlation between levels LDL and WC/HC ratio was demonstrated (r: 0.54 p = 0.003) in FHE and FHO groups. We observed an increase in diastolic blood pressure in the FHO and FNO groups in relation to the FNE and FHE groups (p = 0.010). When we evaluated the cardiac sympathetic modulation (LF‐PI), we observed a significant increase in the FNO and FHO groups when compared to the FNE group (p = 0.0001). Furthermore, the FHO (2.30 ± 0.8) and FHE groups (2.52 ± 1) presented higher cardiac sympato‐vagal balance (LF/HF) compared to FNO (1.85 ± 0.67) and FNE groups (2.01 ± 0.84) (p =0.04). We observed an increase in systemic hydrogen peroxide concentration in the FHO group when compared to the other groups (p=0.003). Moreover, there was an increase in NADPH oxidase in plasma in FNO and FHO groups in relation the FNE and FHE groups (p = 0.04). In addition, there was an increase in plasma nitrite levels in FHO group compared to FNO, FNE and FHE groups (p=0.01). In conclusion our findings demonstrated that despite young and apparently healthy, the group with overweight and FH showed early impairment in HRV and in markers of oxidative stress. In addition, this group presented all dysfunctions observed in the presence of these risk factors alone, which may be associated with increased cardiovascular risk and target organ damage in this population.Support or Funding InformationUNINOVE, CNPq, CAPES, FAPESP.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Mechanisms Underlying Obesity‐Related Hypertension: An Experimental Weight Gain Study in Humans
Authors: McEniery Carmel M , Middlemiss Jessica , Maki‐Petaja Kaisa , Wilkinson Ian 
Published: June 2021

BackgroundThe association between body size and blood pressure (BP) is well recognised. However, not all overweight individuals have elevated BP suggesting that important adaptive mechanisms are present in some. Cardiac output (CO, a key determinant of BP, is elevated in young overweight individuals, but is not associated with the level of BP. However, peripheral vascular resistance (PVR) is associated with the level of BP in these individuals, suggesting that the ability to modulate PVR in response to increased CO is important.ObjectiveWe hypothesized that weight gain increases CO in healthy humans and that the ability of the peripheral vasculature to adapt to this increase determines BP. Therefore, we undertook an exploratory study of experimental weight gain in healthy young adults.MethodsSixteen healthy non‐obese males were recruited (mean±SD age 29±6 years). All participants were overfed approximately 1000kcal/day, alongside their normal diet, for 6–8 weeks, until a weight gain of 5kg was achieved and held stable for at least 1 week. Detailed anthropometric characteristics, BP, CO and PVR were assessed at baseline and at completion of the overfeeding intervention.ResultsOverfeeding resulted in a significant increase in body weight (6.11±3.08kg, P<0.001), lean mass (3.61±3.40kg, P=0.001) and fat mass (2.64±2.89kg, P=0.002). The increases in systolic BP (2±9mmHg) and diastolic BP (2±6mmHg) were not significant (P<0.2 for both) and the increase in heart rate was of borderline significance (5±10bpm, P=0.055). As hypothesised, there was a significant increase in cardiac output (0.81±1.35L/min, P=0.031), which was accompanied by a decrease in PVR (129±205dynes.sec.cm5, P=0.024). Dichotomising individuals on the basis of a systolic BP response to weight gain of ≥5mmHg (BP responders) revealed small differences vs non‐responders in the change in CO (+1.34±0.99L/min vs +0.4±1.50L/min) and PVR (−111±142 dynes.sec.cm5 vs −143±251 dynes.sec.cm5), although neither comparison was statistically significant.ConclusionsModest weight gain in healthy, non‐obese men is associated with an increase in both lean and fat tissue mass. A compensatory reduction in PVR in response to elevated cardiac output is likely to explain the lack of change in BP. Examining ‘responders’ versus ‘non responders’ in terms of BP change in response to weight gain is likely to provide useful insights into obesity‐associated hypertension in a larger trial.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Amoxicillin‐responsive alterations in commensal gut microbiota are associated with lowering of blood pressure in young hypertensive rats
Authors: Galla Sarah L , Chakraborty Saroj , Cheng Xi , Yeo Ji‐Youn , Mell Blair , Joe Bina 
Published: June 2021

Pediatric hypertension is recognized as an emerging global health concern. While new guidelines are developed for facilitating clinical management, the reasons for the prevalence of hypertension in children remain unknown. We hypothesized that, similar to the known link between gut microbiota and adult hypertensives, alterations in gut microbiota that occur very early in childhood are also associated with an increased prevalence of pediatric hypertension. To test this hypothesis, we administered amoxicillin, the most commonly prescribed antibiotic to pediatric patients, to clear gut microbiota of just‐weaned, genetically hypertensive Dahl Salt‐Sensitive (S) rats. Amoxicillin treated rats had decreased BP compared to controls. This lowering effect on blood pressure persisted even after the antibiotics were discontinued. Results will be presented on the specific alterations in gut microbiota in response to amoxicillin treatment. Albeit in an experimental model, our results demonstrate the significant role of gut microbiota in the early development of hypertension and indicate that clearing dysbiotic gut microbiota early in childhood may have long‐term benefits for hypertension‐prone individuals.Support or Funding InformationFunding for this work to BJ from the NHLBI/NIH (HL143082) is gratefully acknowledged.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Varying frequency and pulse width duration during electrical stimulation of cervical sympathetic chain in Zucker Fat rats dramatically alters hemodynamics
Authors: Hsieh Yee‐Hsee , Zenebe Woineshet J , Lewis Stephen J 
Published: June 2021

The influence of electrical stimulation of the cervical sympathetic chain (CSC) on hemodynamics has not been thoroughly investigated. Previous studies using healthy strains of rats focused on upper airway dynamics as well as ventilatory parameters. This current study examined the changes in mean blood pressure (MAP), diaphragmatic electromyogram (EMG), and upper airway pressure (UAP) elicited by electrical stimulation of the CSC in Zucker‐fat rats, a model of obesity‐hypertension,. Under urethane anesthesia, male Zucker‐Fat rats (16 weeks of age, n=4), were instrumented to continuously record MAP, diaphragmatic EMG), and UAP. Both CSC were dissected, isolated and stimulated at 0.5 mA, with varying frequency (2.5, 5, 7.5, 10 and 20 Hz) and pulse widths duration (0.1, 0.2, 0.5 and 2.0 ms). Both frequency and pulse‐width dependent depressor response was observed with bilateral CSC stimulation. Lower frequency stimulations produced a 5% decrease in MAP and 12% decrease in UAP whereas the highest frequency of 20 Hz (0.5 mA, 0.2 ms kept constant) produced a 20% decrease in MAP and 25% decrease in UAP relative to baseline (panel A). The smallest pulse width (0.1 ms) produced a 3% decrease in MAP and 5% decrease in UAP whereas 2 ms produced a 25% MAP drop and 10% drop in UAP relative to baseline measures (panel B). Diaphragmatic changes were negligible with CSC stimulation. We conclude that bilateral electrical stimulation of the CSC effectively lowers MAP and UAP in an obesity‐hypertension rat model. In addition, both frequency and pulse width parameters can vary the hemodynamic response dramatically. Future studies will investigate optimal stimulation parameters and whether stimulation can lower hypertension in conscious Zucker‐Fat rats.Support or Funding InformationSupported by NIH1OT2OD023860‐01, Galvani BioelectronicsThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Necessity of the Hypothalamic Paraventricular Nucleus for the Cardiovascular Responses to Activation of Bradykinin‐Sensitive Pericardial Afferents
Authors: Martin Doug , Reihe Casey 
Published: June 2021

Sympathetic drive is a major controller of cardiovascular function. While the arterial baroreceptors are known to regulate sympathetic drive to the cardiovascular system, other reflex mechanisms also play a role. The heart itself has an important sensory function via a variety of cardiac receptors that modulate cardiovascular responses by both neural and humoral reflexes. Bradykinin‐sensitive sympathetic afferent nerves from the heart can trigger marked increases in efferent sympathetic nerve activity to some cardiovascular target organs such as the kidney, arteries and veins. We reported previously that activation of the hypothalamic paraventricular nucleus (PVN) triggers an increase in arterial pressure, venous tone and cardiac output. This work tested the hypothesis that the PVN is necessary for the cardiovascular responses to activation of bradykinin‐sensitive pericardial afferents.Sprague Dawley rats were anesthetized with a cocktail of alpha chloralose (80 mg/kg) and urethane (800 mg/kg). Catheters were placed in the femoral artery and vein to record arterial and venous blood pressures. The rats were placed in a stereotaxic frame and bilateral guide cannulae were implanted toward the PVN and cemented in place. A PE 10 catheter was placed in the pericardial space for the injection of bradykinin (BK; 1 μg/kg), an agent known to stimulate cardiac sympathetic afferents. The chest was closed and the rat allowed to breathe spontaneously. After recovery from these surgical interventions, the cardiovascular responses to pericardial injection of BK were recorded following PVN injection of vehicle or omega‐conotoxin (1 ng/nl; 200 nl), an N‐type calcium channel antagonist to impair neurotransmission in the PVN.Pericardial injection of BK following PVN injection of vehicle was associated with increases in mean arterial pressure (19±2 mm Hg) and heart rate (7±2 bpm). PVN injection of conotoxin did not markedly affect baseline arterial pressure or heart rate. However, after injection of conotoxin into the PVN, the pressor responses to pericardial injection of bradykinin were markedly attenuated (MAP: − 17±5 mm Hg; HR: −10±4 bpm).We interpret these data to indicate that neurotransmission in the PVN is required for the cardiovascular responses to activation of bradykinin‐sensitive pericardial afferents.Support or Funding InformationSupported by NIH R01 HL136741‐02, the Sanford School of Medicine Medical Student Summer Research Program and the Basic Biomedical Sciences program of the Sanford School of Medicine.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Orexin A receptor 1(OX1R) activation increases expression of cytokines in PC12 cells
Authors: Alharbi Wafa Fhad , Bigalke Jeremy , Chen Qing‐Hui , Shan Zhiyang Jenny 
Published: June 2021

Orexin A is a multifunctional neuropeptide that regulates arousal, wakefulness, appetite and cardiovascular function. Orexin A exists its function through binding with orexin receptor 1 (OX1R) or orexin receptor 2 (OX2R). However, the downstream signal transduction pathway that orexin system mediated is not well determined. In this study, we investigate the hypothesis that binding of orexin A and OX1R results in activation of extracellular signal‐regulated kinase 1 & 2 (ERK1/2) and subsequently increases in inflammatory cytokines. We test this hypothesis using the neuron‐like PC12 cell which artificially expressing human OX1R. Incubation of human orexin A (100 nM) resulted in a time dependent increase in phosphorylated ERK1/2 (P‐ERK1/2) as well as the mRNA levels of Junb, a subunit of transcription factor AP‐1; leukemia inhibitory factor (LIF), and C‐C motif chemokine ligand 2 (CCL2), in PC12‐OX1R cells. The maximum increase in Junb was observe in 3 hours, while the maximum increase in LIF (18.3‐fold) and CCL2 (12.8‐fold) was observed in 6 hours following orexin A treatment. There was no significant increases in P‐ERK1/2, Junb, CCL2 and LIF was observed in orexin A treated PC12‐OX2R cells or PC12 cells. Pre‐incubation of orexin A (100 nM) with PD98059, a blocker for ERK1/2 phosphorylation, dramatically attenuated the expression of Junb, LIF and CCL2 in PC12‐OX1R cells. Our results suggested that activation of orexin system activity may though activation or ERK1/2 in turn stimulate AP1‐cytokine signaling.Support or Funding Information[Grant support: NIH R15HL129213 (Shan), Michigan Technological University and Portage Health Foundation research Excellence Fund]This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.