bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of fragrance inhalation of essential oil on control of blood pressure and muscle sympathetic nerve activity in humans
Authors: Kawai Eriko , Hanno Genta , Takeda Ryosuke , Ota Akemi , Morita Emiko , Imai Daiki , Suzuki Yuta , Yokoyama Hisayo , Okazaki Kazunobu 
Published: June 2021

AimsWe recently reported that inhalation of fragrance of Grapefruit essential oil increased blood pressure (BP) while that of Marjoram essential oil decreased BP in humans. In this study, we investigated the effects of fragrance inhalation of Grapefruit and Marjoram essential oil on control of BP and muscle sympathetic nerve activity (MSNA), and also cardiovagal and sympathetic baroreflex function.MethodsThirteen healthy subjects participated in each trial of this study. The experiment was performed in the supine position. Subjects breathed blank air through a face mask for 10 min as baseline. Then, they inhaled air with the fragrance of Grapefruit or Marjoram essential oil from Douglas bags for 10 min. Throughout the trial, MSNA (peroneal nerve, microneurography), beat‐by‐beat heart rate and BP, and breath‐by‐breath respiratory variables were recorded continuously.ResultsBy inhalation of the fragrance of Grapefruit essential oil, diastolic BP increased at 8 to 10 min of inhalation (64 ± 9 mmHg) compared to baseline (62 ± 9 mmHg), whereas MSNA burst rate remained unchanged at the period of inhalation (14.2 ± 8.5 bursts/min) from baseline (13.2 ± 7.0 bursts/min). Cardiovagal (10.8 ± 5.6 vs. 11.9 ± 9.6 ms/mmHg) or sympathetic baroreflex sensitivity (−0.84 ± 0.61 vs. −1.03 ± 0.78 au/mmHg) remained unchanged from baseline at the period of inhalation. On the other hand, by inhalation of the fragrance of Marjoram essential oil, diastolic BP increased at 8 to 10 min of inhalation (61 ± 7 mmHg) compared to baseline (60 ± 8 mmHg) against our previous studies, while MSNA burst rate remained unchanged at the period of inhalation (14.0 ± 8.5 bursts/min) from baseline (12.0 ± 9.4 bursts/min). Cardiovagal (12.0 ± 7.3 vs. 14.9 ± 13.1 ms/mmHg) or sympathetic baroreflex sensitivity (−1.06 ± 0.65 vs. −0.97 ± 0.54 au/mmHg) remained unchanged from baseline at the period of inhalation. Heart rate and respiratory variables remained unchanged in both trials.ConclusionsThe fragrance stimulation of Grapefruit essential oil increased BP without increase in MSNA nor modulating cardiovagal and sympathetic control of BP in humans.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Role of A1 and A2B Adenosine receptors in Angiotensin II dependent hypertension in mice.
Authors: Yadav Vishal R. , Zhou Zhichao , Teng Bunyen , Mustafa S. Jamal S. 
Published: June 2021

Our recent finding showed that acute angiotensin (ANG) II stimulation enhanced A1 adenosine receptor (AR) dependent cytochrome P450 (Cyp) 4A mediated contraction in mouse mesenteric arteries (MA). In addition, A2BAR dependent and partly KATP channel mediated relaxation was reduced. These data suggest a possible interaction between ANG II and ARs at a vascular level, which may play a role in ANG II dependent hypertension (Yadav et. al. Br J Pharmacol. 2015).We used ANG II (1000 ng/kg/min, 28 days) infused mouse model of hypertension in WT, A1 and A2B AR KO mice. Non‐invasive tail cuff method was used to measure mean arterial blood pressure (MABP). Aorta as a conduit and MA (second order) as a resistance artery were chosen for muscle tension studies. Protein expression in aortas and MAs were analyzed by western blot.Infusion of ANG II increased MABP in mice. Particularly, in ANG II infused WT mice, MABP (mmHg, mean ± SE) at day 0 was 77.1 ± 1.7 which increased to 119.9 ± 5.6 on day 28 (p<0.05). Importantly, in A1 and A2B KO mice, increase in MABP was significantly attenuated. At day 28, in A1AR KO ANG II mice MABP was 98.5 ± 6 and in A2B KO ANG II mice was 96.3 ± 6.8.Higher expression of A1AR (~155%) and Cyp4A (~50%) was noted in hypertensive MAs compared to control. Expression of A1AR and Cyp4A was significantly increased in WT aorta of hypertensive and control mice.In MAs, CCPA‐induced contraction was reduced in hypertensive mice but NECA induced relaxation was comparable. Pinacidil (KATP channel opener) induced relaxation was significantly lower (−25% at 100 nM) in MAs of hypertensive mice. Importantly, in A1 and A2BAR KO mice MAs, pinacidil induced responses were comparable in control and ANG II groups. CCPA (A1AR agonist) ‐induced concentration (% PE) was reduced (~15% at 100 nM, p<0.01) in aorta of hypertensive mice compared to control. NECA, non‐selective AR agonist, produced higher (~ −15% at 10 μM, p<0.05) relaxation in aorta of hypertensive mice. Our histological analysis of aorta showed significantly reduced elastin to collagen ratio and higher media to lumen ratio suggesting vascular remodeling in ANG II hypertensive mice.In conclusion, our data revealed important roles for A1 and A2B AR dependent signaling in ANG II induced hypertension. Reduced pinacidil induced relaxation of resistance arteries may aid vascular contraction and blood pressure. Further studies involving pharmacological inhibitors and genetic models (ANGII KOs) are required to understand the interaction between ANG II and ARs at vascular level in the development of hypertension.Support or Funding InformationSupported from NIH grant HL 027339.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Chronic High Salt Intake Reduces Protein Expression of Tumor Necrosis Factor‐alpha Receptor Type 1 in Renal Cortical Tissue of Mice Lacking the Gene for Endothelial Nitric Oxide Synthase
Authors: Majid Dewan Syed Abdul , Prieto Minolfa C. , Chamberlain Cameron M. , Castillo Alexander 
Published: June 2021

As tumor necrosis factor‐alpha (TNF‐α) induces natriuresis via activation of its receptor type 1 (TNFR1), its mechanistic role in the development of salt sensitive hypertension (SSH) is not yet clearly defined. We have shown earlier that chronic high salt (HS) intake increase, but non‐specific pharmacological inhibition of nitric oxide synthase (NOS) isoforms decreases TNFR1 protein expression in the kidney. Here we examined the hypothesis that such decrease in TNFR1 protein expressions are specific to inhibition of the endothelial isoform of NOS (eNOS), which is the main isoform linked to the development of SSH. Experiments were performed in mice lacking the gene for eNOS (eNOSKO) as well as in wildtype (C57BL6) mice (n=6–7 in each group; 8–9 weeks of age) chronically fed either normal (NS; 0.4% NaCl) or HS (4% NaCl) containing diet for 3 weeks. Systemic BP had measured using tail‐cuff plethysmography and urine collections for 24 hours had performed using metabolic cages at the start of the experiment and at the end of every week during the experimental period. After sacrificing the mice at the end of the treatment period, the kidneys were isolated and processed for tissue analysis. Immunohistochemical analysis of TNFR1 and TNFR2 protein expressions in renal cortical tissues had performed using appropriate antibodies. The staining as well as intensity of TNFR1 and TNFR2 immunoreactivity in renal cortical sections had analyzed using NIS Elements Software AR, which allowed a computerized determination of the area of positive staining and the intensity of immunoreactivity. In the basal condition, the mean BP in eNOSKO mice was higher (89± 0.8 vs 76 ±2.1 mmHg) than that in WT mice. There is no change in BP after 3 wks of NS or HS intake in WT, but HS intake for similar period in eNOSKO increased BP (107±3.6 vs 88 + 0.9 mmHg) compared to the baseline value. As expressed in percent area of positive staining, it was observed that TNFR1 immunoreactivity is lower in eNOSKO mice compared to WT mice both in NS (1.4± 0.2% vs 2.7± 0.6%; P<0.05) and HS (1.8± 0.2% vs 4.1 ± 0.5%; P<0.01) intake conditions. The intensity of TNFR1 immunoreactivity also showed the similar results. However, TNFR2 immunoreactivity was minimal in both strains of mice. Collectively, these data indicate that TNFR1 activity is downregulated in the kidney in the condition of eNOS deficiency that minimizes sodium excretion during HS intake leading to the development of SSH induced by oxidative stress conditions.Support or Funding InformationCOBRE‐ P30GM103337 & Tulane Bridge FundThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Nitric Oxide and Sympatholysis in Rat Soleus Feed Arteries
Authors: Whitaker Madelyn , Heckle Tanner , Jasperse Jeffrey 
Published: June 2021

Previous evidence indicates that nitric oxide (NO), acidity, and ATP may all mediate functional sympatholysis. First, we hypothesized that in rat soleus muscle feed arteries, sympatholytic NO is released from vascular endothelial cells by increased shear stress and acts through a guanylyl cyclase intracellular signaling pathway. Second, we hypothesized that NO, acidity and ATP would inhibit sympathetic signaling in a cumulative fashion. Soleus feed arteries (n = 12 per group) were isolated from male Sprague‐Dawley rats and cannulated on two glass micropipettes for in vitro videomicroscopy. We measured the constriction response to the adrenergic agonist phenylephrine (PE; 10−9 M to 10−4 M, 0.5 log increments) in the presence of varying levels of the nitric oxide donor sodium nitroprusside (SNP; 0 nM, 100 nM and 100 mM), shear stress (0 dy/cm2, 25 dy/cm2, and 135 dy/cm2), SNP + ODQ (30 mM), an inhibitor of guanylyl cyclase, and ATP (1 mM and 100 mM) and decreased pH (7.1 and 6.5). SNP reduced constriction to PE in a dose‐dependent manner (maximum constriction 77.3 % vs. 70.7 % and 56.7 %), indicating that NO interferes with sympathetic constriction. ODQ restored PE‐induced constriction (PE alone 77.5%; with SNP 67.6%; with SNP + ODQ 83.5%), indicating that NO causes sympatholysis through a guanylyl cyclase signaling pathway. However, shear stress did not reduce constriction to PE (67.6 % vs. 68.1 %, and 67.6 %), indicating that increased shear stress during exercise is not the source of the NO causing sympatholysis. Finally, SNP alone reduced constriction to PE (maximum constriction 77.3% vs. 70.7% and 56.7%) as much as SNP + low pH (83.5% vs. 71.4% and 59.1%) or SNP + ATP + low pH (75.7% vs. 70.1% and 61.6%), indicating that these sympatholytic agents do not have a cumulative sympatholytic effect. We conclude that nitric oxide acting through guanylyl cyclase causes sympatholysis, but the source of the nitric oxide during exercise is not shear stress‐induced endothelial cell activation.Support or Funding InformationDee Anna Smith Fund for Women in STEM and the Seaver Research Council of Pepperdine University.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
GsMTx4 Reduces the Pressor Response during Dynamic Hindlimb Muscle Stretch in Decerebrate Rats
Authors: Sanderson Bailey C. , Rollins Korynne S. , Kempf Evan A. , Hopkins Tyler D. , Butenas Alec L. , Ade Carl J. , Copp Steven W. 
Published: June 2021

The exercise pressor reflex, which is activated by mechanical and metabolic stimuli arising from within contracting skeletal muscles, contributes to the increase in blood pressure that occurs during exercise. GsMTx4, a mechano‐gated channel inhibitor that is partially selective for piezo channels, was recently found to reduce the pressor response during static rat hindlimb muscle stretch, a maneuver that is commonly used to study the mechanical component of the exercise pressor reflex. However, the GsMTx4‐induced reduction of the pressor response was limited to the initial phase (i.e., the first ~5 sec) of the stretch when muscle length was changing. That finding may reflect the rapid deactivation kinetics of piezo2 channels and the possibility that they do not contribute importantly to the later phases of a static stretch when muscle length is not changing. To investigate this possibility, we tested the hypothesis that in decerebrate, unanesthetized rats, GsMTx4 would reduce the pressor response throughout the duration of a 1 Hz dynamic hindlimb muscle stretch protocol that produced repeated changes in muscle length. Young adult male Sprague‐Dawley rats (n=12) had a jugular vein and both common carotid arteries cannulated. The left calcaneus was cut and the triceps surae muscles were linked by string to a force transducer. The pressor response during 30 seconds of 1 Hz dynamic stretch was measured before and after the injection of 10 μg of GsMTx4 into the arterial supply of the left hindlimb. We found that GsMTx4 reduced the peak pressor response during dynamic stretch (control: 15±4, GsMTx4: 5±2 mmHg, p=0.047, n=7). Moreover, the effect of GsMTx4 on the pressor response was evident throughout the duration of the dynamic stretch protocol. GsMTx4 did not, however, reduce the pressor response that resulted from the hindlimb arterial injection of 24 mmol lactic acid (control: 32±5, post‐GsMTx4: 29±4 mmHg, p=0.53) which indicates that GsMTx4 did not block voltage‐gated sodium channels in our experiments. Furthermore, the injection of GsMTx4 into the jugular vein (n=5) had no effect on the pressor response during dynamic stretch (control: 19±6, GsMTx4: 19±4, p=0.98). This finding indicates that when GsMTx4 was injected into the arterial supply of the hindlimb its effect on the pressor response during stretch was due to its actions on the peripheral endings of the sensory neurons. Our present findings suggest that piezo channels, most likely piezo2 channels, contribute to the pressor response throughout the duration of dynamic hindlimb muscle stretch in decerebrate rats.Support or Funding InformationSupported by university/departmental fundsThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Duration Dependent Effects of Intermittent Hypoxia (IH) on Adult Hippocampal Neurogenesis
Authors: Nallamothu Thara , Khuu Maggie A. , Garcia Alfredo J. 
Published: June 2021

Patients with sleep apnea commonly exhibit cognitive decline and injury to the hippocampal formation. Rodents exposed to IH, a primary consequence of the condition, also show impaired hippocampal based learning and memory. While these impairments correlate with suppressed long‐term potentiation, synaptic plasticity is only one process that supports normal function in this brain structure. Adult neurogenesis is also important for maintaining normal hippocampal physiology. Although Hypoxia Inducible Factor 1a (HIF1a) signaling is to important cellular development and homeostatic responses to hypoxia, chronic IH‐dependent HIF1a activity can promote pathophysiology. In this ongoing study, we test the hypothesis that IH causes HIF1a dependent signaling in neural stem cells (NSCs) to disrupt the adult neurogenesis. To follow the fate of wildtype NSCs and NSCs heterozygous for HIF1a (HIF1a+/−), we used a birth labeling strategy in transgenic mice. After labeling NSCs, we exposed mice to 0 (control), 10, or 30 days of IH. Tissue was harvested for immunohistochemical study at the 33 to 35 day time point. Relative to control, 10 days of IH increased the proportion of GCs generated from wildtype NSCs (by 23% ± 1% SEM, n=3); whereas, 30 days IH suppressed this proportion (−9% ± 2% SEM, n=2). Sholl analysis showed dendritic complexity was similar across all wildtype GCs. 30 days IH exaggerated the loss of GCs generated from HIF1a+/− NSCs (by −30% ± 5%, n=3). These findings indicate that IH has duration‐dependent effects on adult neurogenesis that impact the terminal differentiation of NSCs to GCs and involves IH‐dependent HIF1a signaling in NSCs. These findings suggest that IH‐dependent HIF1a signaling has both positive and negative effects on adult neurogenesis. This mechanism could be a contributor to the negative effects on learning and memory commonly seen in sleep apnea patients.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Progesterone induced blocking factor improves fetal growth restriction possibly by reducing inflammation and placental cytolytic NK cells in response to placental ischemia during pregnancy
Authors: Amaral Lorena M. , Cottrell Jesse N. , Cornelius Denise C. , Cunningham Mark W. , Ibrahim Tarek , LaMarca Babbette 
Published: June 2021

Preeclampsia (PE), new onset hypertension, is a progesterone deficient state and is associated with an imbalance among CD4+ T lymphocytes, natural killer (NK) cells, and inflammatory cytokines which are likely culprits for decreased fetal weight during PE pregnancies. During normal pregnancy activated lymphocytes express progesterone receptors, which enable progesterone to induce a protein called progesterone induced blocking factor (PIBF). PIBF increases during normal pregnancy and has been shown to decrease inflammation and cytolytic NK cells, both of which are increased during PE. Currently, there is no effective treatment for PE except for early delivery, making PE the leading cause for premature births worldwide. We have previously shown that progesterone supplementation with 17‐OHPC improves inflammation, fetal weight and blood pressure in the preclinical RUPP rat model of PE. However the mechanism where by progesterone improves the pathophysiology of PE has never been determined. This study was designed to test the hypothesis that PIBF reduces inflammation while improving hypertension in response to placental ischemia. To test this hypothesis, PIBF (2.0 μg/mL) was administered intraperitoneally on gestation day 15 to RUPP or normal pregnant (NP) rats and on day 18 carotid catheters were inserted and on GD 19 blood pressure and samples were collected. MAP in NP rats (n=9) was 102± 3 and 110 ± 3 in NP+PIBF (n=5), 124± 3 in RUPP rats (n=4), which improved to 110±3 mmHg in RUPP+PIBF (n=8), p<0.05. Pup weight was 2.4± 0.1 g in NP, 2.5± 0.1 in NP+PIBF, 1.9±0.1 in RUPP and improved to 2.2±0.1 in RUPP+PIBF, p<0.05. Total placental NK cells were 31± 9 in NP (n=4), 31±5 in NP+PIBF (n=4), 42 ±8 in RUPP rats (n=4) and reduced to 26± 2 in RUPP+PIBF (n=6). Placental cytolytic NK cells were 0.8±0.1 in NP, 0.2±0.1 in NP+PIBF, and 1.4±0.1 in RUPP rats, which decreased to 0.4+0.1 in RUPP+PIBF, p<0.05. CD4+ T cells were decreased from 21±6 in RUPP rats (n=4) to 8±2 gate in RUPP+PIBF (n=7). Collectively, our findings demonstrate that PIBF, a produce to progesterone receptor stimulation by progesterone, could be a mechanism to improve fetal growth restriction, inflammation as indicated by CD4+ T cells and cytolytic NK cells while normalizing blood pressure in response to placental ischemia during pregnancy.Support or Funding InformationSupported by NIH grants RO1HD067541, HL130456 and AMAG PharmaceuticalsThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Hippocampal CA1 Neuronal and Sympathetic Nerve Activities in Response to Restraint Water‐Immersion Stress in Conscious Rats
Authors: Nagao Kana , Ukita Hiroka , Yoshimoto Misa , Miki Kenju 
Published: June 2021

The hippocampus has been suggested to play a significant role in adaptation to chronic stress. However, there has been lack of direct evidence for responses of hippocampal neuronal activity to chronic stress. The present study was aimed to record hippocampal CA1 neuronal and sympathetic nerve activities during chronic stress. Wistar rats were instrumented chronically with a combined probe made with multiple electrodes (100 micrometer stainless steel wires) for measurement of hippocampal CA1 neuronal activity and glass fiber for measurement of hippocampal cerebral blood flow (CBF), electrodes for measurements of renal (RSNA) and lumbar (LSNA) sympathetic nerve activity, and electroencephalogram, electromyogram, and electrocardiogram and with catheter for measurement of systemic arterial pressure (AP). Rats were exposed repeatedly to restraint water‐immersion stress (RWIS) for 90 min/day over 5 days. Hippocampal CA1 neuronal activity, RSNA, and LSNA were measured continuously and simultaneously before, during, and after RWIS. Hippocampal CA1 neuronal activity decreased immediately after onset of RWIS and the decreased level was maintained throughout the 90 min of RWIS on the first day of stress exposure. On day 5 of RWIS, hippocampal CA1 neuronal activity decreased immediately after onset of RWIS, however it gradually recovered to the control level during the RWIS period. Thus, hippocampal CA1 neurons gradually adapted to the repeated RWIS exposure while RSNA and LSNA increased immediately after the onset of RWIS and showed no adaptive response during repeated exposure to RWIS.Support or Funding InformationJSPS GrantThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
MASP‐3: a new leptomeningeal protein in the lectin pathway
Authors: Dorta‐Contreras Alberto Juan , Padrón‐González Alexander Ariel , González‐Losada Cristobal , Lumpuy‐Castillo Jairo , Rodriguez‐Pérez Jose Alejandro , Ramos‐Robledo Alejandro , Martínez‐Reyes Josue , Schmitz Matthias , Zerr Inga , Hansen Anette Gudmann , Jensenius Jens Christian 
Published: June 2021

IntroductionMASP‐3, a protein of the innate immune response is attracting increasing interest, in particularly in relation to its regulatory function in the lectin pathway.ObjectiveProvide data that discriminate the source of MASP‐3 in cerebrospinal fluid.Materials and methods60 serum and cerebrospinal fluid samples from normal controls without organic disease with normal barrier function were obtained. MASP‐3 was assayed in samples of cerebrospinal fluid and serum with an ELISA, coated with anti MASP‐3 antibodies. It takes into account three variables: the molecular size‐dependent concentration gradient between CSF and blood, the variation in transfer between blood and CSF, and the CSF MASP‐3 concentration correlation with the albumin CSF/serum quotient (Qalb), i.e., with CSF flow rate.ResultsMASP‐3 concentration in CSF was lower than its serum concentration but MASP‐3 concentration in CSF was at least three‐fold higher than expected for a molecular‐size dependent passage from blood. The smaller inter‐individual variation of MASP‐3 concentrations in CSF of the control group (CV =0,396) compared to the MBL concentrations in serum (CV=0.413) indicate an independent source of MASP‐3 in CSF. The absolute MASP‐3 concentration in CSF increases with increasing Qalb. Among brain‐derived proteins in CSF only the leptomeningeal proteins showed a (linear) increase with decreasing CSF flow rate in comparison to neuronal and glial proteins that are invariant to changes of Qalb.ConclusionsMASP‐3 in CSF is predominantly brain‐derived and all results pointed to the leptomeningeal cells as the source of the protein.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.