bluuebunny/crossref_metadata_2025_split huggingface dataset:
Central Autonomic Nervous System Balanced by Electroacupuncture in Hypertension
Authors: Tjen-a-Looi Stephanie , Gong Yiwei , Fu Liang-Wu , Guo Zhi-Ling , Nguyen Anh , Malik Shaista 
Published: May 2023

Overexcitation of sympathetic activity strongly related to increased blood pressure (BP) is decreased by electroacupuncture (EA). Reflex elevated BP response and elevated neuronal activity in the rostral ventrolateral medulla (rVLM), a central region for sympathetic outflow are reduced by stimulation of somatosensory nerves during a 30 min EA. However, it is unclear if the medullary nucleus ambiguus (NA) related to parasympathetic activity also is influenced by EA during elevated BP. In hypertensive subjects, EA therapy over deep peroneal and tibial nerves (ST36-37+SP6-7) decreases high BP. We hypothesize that a course of EA treatments decreases high BP by reducing rVLM and simultaneously increasing NA neuronal activity in hypertensive rats. Dahl salt-sensitive rats were fed either a standard rat diet or 4% salt rat diet developing hypertension. Normotensive control rats were acclimated to handling and restraining while Sham-EA (absence of electrical input to acupuncture needles) and EA treated hypertensive rats were acclimatized also to needling. Sham-EA or EA was given twice a week for 30 minutes in awake hypertensive rats for 5 weeks. BPs were measured with tail-cuff CODA system. At end of 10 weeks, tyrosine hydroxylase (TH) and choline acetyltransferase (ChAT) neuronal (NeuN) expressions were evaluated by immunohistochemistry as well as neuronal activity were determined by extracellular recordings in the rVLM and NA in Sham-EA, EA treated rats, and control rats. BP of control rats was at 130.3±1.7 mmHg (n=6) at end of experiment. BP significantly decreased by 25.9% in EA treated (138.04±1.8 mmHg, n=6) compared to Sham-EA (186.3±2.3 mmHg, n=7) hypertensive rats. Cardiovascular pre-sympathetic neuronal activity in rVLM significantly was decreased by 43% (1.33±0.10 to 0.75±0.13 sp/s, n=10) while the pre-parasympathetic activity in NA was increased by 96% (0.70±0.08 to 1.37±0.13 sp/s, n=12) in EA compared to Sham-EA treated hypertensive rats. Control rats rVLM activity was 0.23± 0.07 sp/s (n=4) and NA activity was 2.71±0.56 sp/s (n=5). Also, numbers of rVLM neurons expressing TH and NeuN were decreased (from 96 to 73) and NA neurons expressing ChAT and NeuN were increased (from 35 to 107) in Sham-EA compared to EA treated hypertensive rats. In normal control rats, rVLM showed 69 TH neurons and NA demonstrated 134 ChAT neurons. In conclusion, the BP lowering EA effect likely involved central autonomic rebalance by activating both sympathoinhibition and parasympathoexcitation. National Institute of Health National Center for Complementary & Integrative Health Grant AT011306 This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.
The gut microbiome and inflammation in the BPH5 preeclamptic like mouse model
Authors: Beckers Kalie , Schulz Christopher , Flanagan Juliet , Childers Gary , Sones Jenny 
Published: May 2023

Preeclampsia (PE) is a life-threatening hypertensive disorder of pregnancy. It occurs in ~10% of pregnant women worldwide and the etiology is still unknown. Obesity increases the risk of developing PE by three-fold and has been associated with adverse fetal outcomes. Short chain fatty acids (SFCAs) are gut microbiome derived metabolites that fuel the host metabolism and have been found to be key mediators between dysbiosis and disease signaling through G protein coupled receptors (GPRs) that regulate appetite and glucose metabolism. We hypothesize that obese mice with a gut dysbiosis have perturbed GPR pathways and increased local inflammatory response. To better understand the relationship of maternal PE risk and outcomes, the obese hypertensive BPH/5 mouse model of superimposed PE was utilized. Previous research demonstrated that adult BPH/5 female mice have an adverse cardiometabolic phenotype: hyperphagia, hypertension, obesity with increased white adipose tissue (WAT), and dyslipidemia that is exaggerated by pregnancy. Fecal samples were collected from pregnant and non-pregnant BPH5 and C57 female controls for Illumina sequencing of 16S v4 rRNA amplicon libraries to examine the PE-like maternal fecal microbiome. SCFAs, GPR41, and IL-15 were measured in the colon of the pregnant dams. Microbial community composition of the pregnant BPH/5 compared to the lean normotensive C57 controls were significantly different using PERMANOVA with Bray-Curtis dissimilarity of 16S Amplicon Sequence Variant’s relative abundance (p<0.05, n=8-15). Alpha diversity was increased in pregnant BPH/5 dams compared to lean C57 dams (p<0.05, n=8-15). Significant differences were also found in the BPH5 model after the onset of pregnancy such as a decrease in Muribaculum spp., Muribaculaceae unclassified, Parabacteroides spp, and Lachnospiraceae_NK4A136 unclassified. SCFAs were not different between groups (p>0.05). BPH5 demonstrate an altered GPR41 pathway with decreased GPR 41 expression in the colon (p<0.05, n=5-9) and increased IL-15 to represent local colonic inflammation (p<0.05, n=3). In conclusion, the maternal fecal microbiome demonstrates microbial dysbiosis characterized by diversity changes in a model of PE and after the onset of pregnancy. The gut dysbiosis may be a key mechanism that affects GPR41 signaling, inflammation, and contributes to the BPH5 phenotype and poor pregnancy outcomes. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.
Physiological and behavioral responses of northern elephant seals (Mirounga angustirostris) to global change among three northern California rookeries
Authors: Lam Emily , Mouly Maxine , Congdon Cambrie , Henderson Kyra , Vazquez-Medina Jose 
Published: May 2023

The California coast provides a unique study system for investigating the effects of warming and habitat quality on the thermoregulatory capacity of the northern elephant seal (NES). In California, island rookeries such as the offshore site at the Farallon Islands National Wildlife Refuge are experiencing habitat loss and reduced suitable haul-out surfaces due to erosion from storm events. Extreme weather events are increasing in frequency and severity with global change. Semi-aquatic animals face a unique thermal challenge. They possess adaptations to conserve heat when immersed in cold water during deep dives but must compensate for such heat-conserving properties of their physiology when transitioning to heat exposure on land. Therefore, these animals must precisely thermoregulate with physiological and behavioral adjustments across a broad thermal range. We investigated how environmental variables affect seal thermoregulation at three northern California rookeries, the southeast Farallon Island (SEFI), Point Reyes National Seashore (PORE) and Año Nuevo State Park (ANSP). Infrared thermography was used to determine seal skin surface temperature and weather data was collected at each site. We found that average surface temperature increases with solar radiation, maximum surface temperature decreases with increasing wind speed, and thermal window area percentage decreases with relative humidity and increases with ambient temperature. Climatic variation may present physiological and behavioral challenges for marine mammals that experience significant life-history stages on land. Such ongoing findings will be fundamental in predicting climate change vulnerabilities and will be critical in mitigating the impacts of anthropogenic warming and promoting resilience in these populations. Carol Baird Graduate Student Award for Field Research; The Neubacher Fund for Marine Science at Point Reyes National Seashore. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.
Different effects of fenoldopam and angiotensin II on autophagy in vascular smooth muscle cells
Authors: Lee Hewang , Lu Amy , Polzin Jacob , Armando Ines , Jose Pedro 
Published: May 2023

Both dopamine and angiotensin II are essential neurotransmitters/hormones with pleiotropic functions in vascular smooth muscle cells (VSMCs). Autophagy, an intracellular self-degradative process that delivers cytoplasmic constituents to lysosomes, plays an important role in physiological homeostasis in VSMCs. Fenoldopam (Fen), a dopamine D1/D5 receptor agonist, increases autophagic flux in renal proximal tubule cells, however, in VSMCs the roles of these two neurotransmitters on autophagy are unknown. In rat aortic VSMCs, Fen increased autophagy, determined by the protein expression of microtubule-associated protein 1 light chain (LC)3-II and autophagy related 5 (ATG5), in a concentration- and time-dependent manner. By contrast, angiotensin II (Ang II), the endogenous AT1R agonist, decreased the protein expression of LC3-II and ATG5 in a concentration-and time-dependent manner. Further studies showed that Fen (1 μM, 15 min) increased while Ang II (100 nM, 15 min) decreased cyclic AMP (cAMP) production in VSMCs (Vehicle: 100±35.4%, Fen: 513.7±95.8%, Ang II: 24.6±8.0%, n=6). Pre-treatment with Rp-cAMPS (50 μM, 6 hr), a PKA inhibitor, attenuated the Fen-mediated increase in LC3-II protein expression (Fen: 1 μM, 6 hr) (Vehicle: 100±15.0%, Fen: 251.8±37.2%, Fen+Rp-cAMP: 96.9±16.7%, n=6) and reversed the Ang II-mediated decrease in autophagy (Ang II: 100 nM, 6 hr) (Vehicle: 100±8.9%, Ang II: 44.9±6.3%, Ang II+Rp-cAMP: 95.4±11.0%, n=4). These results demonstrate distinct roles of Fen and Ang II on autophagy through regulation of cAMP/PKA signaling by their corresponding receptors in VSMCs. This study was supported by National Institutes of Health of US and National Natural Science Foundation of China. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.
Investigating the metabolic changes that accompany skeletal muscle maturation
Authors: Rimmer Linnea , Geisbrecht Erika , Chao Michael , Woodworth Jason , O'Quinn Travis , Zumbaugh Morgan 
Published: May 2023

Skeletal muscle plasticity is imperative for our overall health but diminishes with inactivity and age. As we reach maturity, a shift in nutrient allocation from supporting skeletal muscle hypertrophy to adipogenesis occurs. This pivotal intersection in tissue growth marks the start of a metabolic decline in skeletal muscle and an accumulation of adipose tissue in inactive individuals. If left uncorrected, a loss of skeletal muscle metabolic flexibility can lead to a myriad of metabolic diseases. To define the metabolic changes in skeletal muscle that accompany maturation, samples were collected from the longissimus dorsi (LD, glycolytic muscle), latissimus dorsi (LAT, mixed muscle), and masseter (MS, oxidative muscle) at 20, 53, 87, 120, and 180 days of age from DNA 600 x 241 (DNA Genetics) castrated male pigs that weighed an average of 5.7, 20.8, 42.2, 83.4, and 130.5 kg, respectively. These ages were selected to correspond to tissue growth phases characterized by vital organ growth, intensive muscle hypertrophy, cessation of muscle hypertrophy, and the beginning of unrestricted adipose deposition. Samples were analyzed to determine the abundance of key metabolic enzymes through Western blotting and assess mitochondrial content through real-time PCR. Glucose-6-phosphate dehydrogenase decreased at 87, 120, and 180 d in MS compared to LAT and LD ( P < 0.01), which suggested glycolytic muscles increased nutrient allocation to the pentose phosphate pathway at this time whereas oxidative muscles did not. Moreover, pyruvate dehydrogenase ( P < 0.01) and citrate synthase ( P < 0.01) increased at 120 d, which indicated an increase in metabolites entering oxidative pathways. This increase was accompanied by an increase in mitochondrial DNA at 87 and 120 d ( P < 0.01). Further, glutamic-oxaloacetic transaminase 2 increased between 20 d to 120 d ( P < 0.01) indicating amino acid synthesis peaks at 120 d. These findings have established a metabolic fingerprint associated with the termination of muscle growth and the beginning of adipose tissue growth, which provides the framework for uncovering the regulatory mechanism that modulates nutrient allocation between muscle and fat. Elucidating this mechanism will aid in the discovery of metabolic interventions to combat metabolic diseases. Kansas State University Global Food Systems Seed Grant Program This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.
Beta-hydroxybutyrate-induced vasodilation is mediated by Kv7 potassium channels
Authors: Hester Seth , Waigi Emily , Costa Tiago , Wilson Emily , Pernomian Laena , Fontes Milene , Wenceslau Camilla , McCarthy Cameron 
Published: May 2023

Despite the conflicting reports on ketogenic interventions at lowering blood pressure and ameliorating hypertension, we have previously demonstrated that the most abundant ketone body, β-hydroxybutyrate (βOHB) is a novel vasodilator. While the G-protein couple receptors, Gpr109 and Gpr41, are the canonical receptors for βOHB, they do not mediate βOHB-induced vasodilation. On the other hand, it has been observed in central nervous system that βOHB can activate potassium channels of the KV7 family such as KCNQ1, KCNQ2, and KCNQ3. In addition, the presence of KV7 channels has been observed in the endothelial cells. Therefore, we hypothesized that βOHB-induced vasodilation was mediated through KV7 potassium channels. To examine this, we analyzed βOHB-induced vasodilation in mesenteric resistance arteries (MRA) of 12-15 week old male Wistar rats (n=4-14) in the presence of three different KV7 inhibitors, Linopiridine dihydrochloride (10-5 M), XE991 dihydrochloride (10-6 M), or 4-Amino-3-hydroxybutyric Acid (10-4 M), using wire myography. We observed that each inhibitor stifled the relaxing effects of βOHB Linopiridine dihydrochloride [AUC control 240 ±31.7, vs. Linopiridine dihydrochloride 74.61 ±26.7, p<0.05], XE991 dihydrochloride [AUC control 240 ±31.7, vs. XE991 dihydrochloride 101.6 ±35.3, p<0.05], and 4-Amino-3-hydroxybutyric Acid [AUC control 240 ±31.7, vs. 4-Amino-3-hydroxybutyric Acid 71.3 ±31.3, p<0.05]. Overall, these data suggest that βOHB propagates vasodilation through non-canonical KV7 channels. Funding: R00GM118885, R01HL149762, R00HL151889, and NHLBI (R00HL151889) This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.
Cardiovascular and renoprotective effects of renal denervation associated with AT1 receptor antagonism in experimental chronic kidney disease
Authors: Veiga Amanda , Campos Ruy , Bergamaschi Cássia , Nishi Erika 
Published: May 2023

Chronic kidney disease (CKD) is characterized by progressive and irreversible loss of kidney function. The main causes of CKD are arterial hypertension (AH) and type 2 diabetes. Previous studies by our group showed that renal denervation (DNx) decreased arterial hypertension and sympathetic overactivity in rats with CKD. In the present study, we studied the renoprotective and cardiovascular effects of DNx associated or not with renin-angiotensin system (RAS) blockade. Wistar rats underwent experimental CKD induction (⅚ nephrectomy model). After 4 weeks of CKD induction, we performed DNx and collected data after 4 weeks. Groups that underwent RAS blockade were treated orally with losartan (30mg/kg/day) in the last 4 weeks of the 8-week protocol. Losartan decreased arterial pressure (118±21 mmHg) compared to CKD group (175±18 mmHg). However, the association of losartan treatment with DNx was able to normalize this parameter (94±9mmHg). In addition, losartan normalized baseline renal sympathetic nerve activity, and DNX associated or not with losartan normalized splanchnic sympathetic nerve activity. Interestingly, lipocalin associated with neutrophil gelatinase (NGAL), an important marker of tubular injury, and an intrarenal RAS marker were normalized after DNx associated with losartan treatment (70.9±23.8 NGAL:Cru) or not (66.6±17.8 NGAL:Cru) was normalized. Treatments unchanged water intake or urinary flow. Taken altogether, our data show that despite the association of DNx and RAS blockade produces a further decrease in AH, the improvement in renal function markers and normalization in intrarenal RAS and sympathetic drive is similar after DNx or RAS blockade alone. FINANCIAL SUPPORT: CAPES, FAPESP and CNPq This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.
Using small group presentation of primary research literature to facilitate understanding and discussion in a graduate neurophysiology class
Authors: Knight Marvar Sarah , Knight Marvar Sarah 
Published: May 2023

In order to stimulate a deeper understanding of physiology concepts in a graduate neurophysiology course, students analyzed and discussed primary research literature in the form of small group presentations. Our aim was to use original research articles to enhance understanding of major concepts and for students to gain historical context of seminal findings in neurophysiology. We hypothesized that giving students the opportunity to discuss the article in small groups, focusing on a specific section then presenting to the class before a large-group discussion would deepen their understanding of the material and build confidence in discussing scientific literature. Students were required to read and submit a short synopsis of a primary research article provided by the class instructor before class. In class, students were separated into groups of between 4-8 and allowed 1 hour to prepare a 5 - 10 minute presentation summarizing a section of the research article, such as the methods section. Following the small group presentations students were encouraged to discuss the findings and implications further. Students reflected on the use of primary research literature in the course and its impact on their learning.In a student survey 76% of students reported feeling more confident in reading, discussing and presenting primary research articles because of this course, whereas just 41% believed that reading primary research articles were a valuable part of the course and improved their understanding of the material. The inclusion of a group presentation of the material to their peers appeared to encourage deeper analysis, discussion and therefore better understanding of the literature. Whether that translated to deeper understanding of the physiological concepts of the class requires further study. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.
Carbon dioxide attenuates PKC signaling and is sensed in monocytes and macrophages by a CA2-dependent, coupled intracellular pH-response
Authors: Strowitzki Moritz J. , Bleul Marc , Tuffs Christopher , Dupovac Mareen , Blanco Alfonso , Cummins Eoin P. , Schneider Martin , Taylor Cormac 
Published: May 2023

Background: Increased levels of CO2 reduce macrophage function during inflammatory processes and wound healing. However, little is known how macrophages sense CO2 and adapt upon high levels of CO2 during differentiation and activation. We, therefore, elucidated the effects of CO2 on gene and protein expression during basic inflammatory processes, such as monocyte differentiation and macrophage activation. Methods: Monocyte differentiation was induced by phorbol 12-myristate 13-acetate (PMA). Primary macrophages (BMDMs) were polarized using different cytokines to induce proinflammatory (M1) macrophages (lipopolysaccharides) or immunomodulatory (M2) macrophages (interleukin-4). Cells were simultaneously subjected to different levels of CO2. Morphological changes, mRNA and protein expression of markers for cell differentiation and macrophage polarization were determined. Cell culture medium was buffered and intracellular pH (pHi) was monitored to determine pH-dependent effects of CO2. Direct effects of CO2 on PKC protein function were analyzed. Results: High levels of CO2 attenuated PMA-induced cell differentiation of human monocytes. In BMDMs, CO2 significantly reduced transcript levels of M1-marker. Mechanistically, CO2 mitigated PMA-stimulated PKC activity and function. Experiments with buffered medium revealed that changes in pH were responsible for most, but not all, of the CO2-mediated effects on monocyte differentiation and macrophage polarization. Pharmacological and genetic inhibition of carbonic anhydrases (CA) uncoupled the CO2-elicited intracellular pH-response, thereby preventing CO2-sensitivity during monocyte differentiation, activation, and migration, which could be reversed by CRISPR-mediated upregulation of CA2. Conclusion: Carbon dioxide is highly immunomodulatory and might thus affect wound healing properties in vivo. In M1 (but not M2) macrophages, CO2 is sensed by CA2-driven changes in pHi. MJS received funding from the German Research Foundation (DFG; STR 1570/1-1) and the Braun Foundation (Braun®; BBST-D-18-00018). This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.