Significant Increase In Systolic Blood Pressure Research Articles

Abstract P426: Reduced Nfatc1 Expression Results in Enhanced Pressure Natriuresis and Resistance to Salt-Sensitive Hypertension

Background: Nuclear factor of activated T cells-cytoplasmic 1 (NFATc1) has recently been shown to have a non-canonical role in chronic kidney disease in humans by a trans-ethnic meta-analysis of genome-wide associate studies (GWAS). Follow-up studies in a salt-sensitive mouse model showed that Nfatc1 mRNA expression was suppressed in the kidneys when animals were fed a high-salt diet. Here, we further explore the link between NFATc1 and salt-sensitive (SS) hypertension. Methods: Adult male wild-type (WT) and heterozygous Nfatc1 knockout (Het) mice (2-5 months of age) on the SS 129S6 background were started on standard chow (0.8% NaCl, NSD) and then switched to a high-salt diet (6% NaCl, HSD). Systolic blood pressure (SBP) was measured by either tail cuff manometry with at least 2 weeks of training or implantable radiotelemetry transmitters with at least 2 weeks of post-surgical recovery. Immediately before and for 2-3 days after the change in diet, 24 h urine was collected using metabolic cages, and urinary sodium was measured by flame photometry. Sigmoid pressure-natriuresis curves were generated and the Hill slope was compared between genotypes. Results: WT mice showed a significant increase in SBP between NSD and after 3 weeks on HSD (127.8±9.9 vs 143.4±8.9, p = 0.0089, n = 9). In contrast, Het mice had no change in SBP (125.8±8.7 mmHg vs. 125.7±10.6 mmHg, p = 1.0, n = 9). During the initial switch to the HSD, SBP was not significantly different between WT and Het mice (133.2±2.9 vs. 134.4±3.0, p = 0.45, n = 7/group). However, WT mice had a shallower pressure-natriuresis curve (Hill slope of 0.58 vs. 0.93, 7 mice/group, 25/26 data points). Conclusion: Our data illustrates that decreasing Nfatc1 expression in a mouse model is protective against SS hypertension. While acute increases in SBP in response to HSD remained in Het mice, sodium excretion was increased and SBP remained unchanged after 3 weeks, indicating that NFATc1 has the potential to be a therapeutic target against SS hypertension.

P109 AMINOPEPTIDASE A: A POTENTIAL NOVEL THERAPY FOR ANGIOTENSIN-DEPENDENT HYPERTENSION?

Background: We have shown that mice with a genetic deficiency in Aminopeptidase A (APA) have elevatedblood pressure. APA is an enzyme that removes a single aspartate residue from the amino-terminus of several peptides in the renin-angiotensin systems (RAS), including angiotensin (Ang) II. In this study, we investigated the impact of a recombinant APA on the cleavage of various RAS peptides and its effect on blood pressure. Methods: An in vitro assay was used to identify Ang peptides as substrates for APA. Ang peptides identified as APA substrates using this assay were then injected to anesthetized WT and APA-deficient mice to assess their pressor effect by measuring systolic blood pressure (SBP). Subsequently, murine recombinant (r)APA was used to evaluate its action on the acute SBP elevation elicited by Ang peptides that were identified to trigger pressor response. Results: In the in vitro assay, Ang II (22427±3353, n=12), Ang I (21883±1692, n=3), Ang1-7 (15833±3395,n=3), Ang1-9 (15773±3395, n=3) and Ang1-12 (13170±220, n=3), were identified as a substrate for rAPA as indicated by a strong aspartate-driven fluorescence formation. When these five Ang peptides were administered to WT mice, only Ang I, Ang II and Ang 1-12 caused a significant increase in SBP. This effect was exaggerated in APA deficient mice. The SBP increase elicited by Ang II in WT mice was markedly reduced by the pre-administration of rAPA (Fig). Conclusion: Aminopeptidase A can cleave the N-terminal aspartate from Ang II as well as from other RASpeptides that elicit (Ang 1-12, Ang I) and do not elicit (Ang 1-9, Ang 1-7) pressor response in mice. APA deficiency is associated with an exaggerated SBP response to Ang I, Ang II and Ang 1-12 while the recombinant enzyme mitigates the acute hypertensive effect. rAPA markedly reduced the increase in SBP caused by AngII infusion suggesting that it may be used to treat hypertension caused by excess of AngII.

Long-lasting effects of post-traumatic stress disorder in Yazidi women living in Northern Iraqi camps

The severity of post-traumatic stress disorder and its long-lasting effects among the Yazidi population has not yet been investigated. ObjectivesThis study evaluated the impact of PTSD severity and chronicity on physiological and anthropometric parameters in women survivors of the genocide-related events after the so-called Islamic State of Iraq and Syria (ISIS) attack in 2014. MethodsThe diagnosis PTSD was assessed using PTSD Checklist for DSM-5 (PCL-5). Participants were divided into: External control (healthy individuals living outside the camps), Internal control (healthy individuals living in the camps), and PTSD group (individuals diagnosed with PTSD). The PTSD group was subdivided according to chronicity <2 years, 2–5 years, and >5 years and subdivided according to PTSD severity into “Moderate”, “Severe” and “Extreme”. Systolic blood pressure (SBP), diastolic blood pressure (DBP), blood oxygen saturation (SPO2) and heart rate (HR) were evaluated. Weight, height and waist circumference were measured. Body mass index (BMI) and waist-to-height ratio (WHtR) were calculated. ResultsThe PTSD group showed significant increases in SBP, DBP, heart rate, BMI, WC, weight, and WHtR compared to the control groups. SPO2 values decreased in the PTSD group. As the disease progressed, there were further increases in SBP, DBP, heart rate, BMI, WC, WHtR, and weight. Similar increases were observed with the severity of the disease. ConclusionOur data indicates that a long-term impact on physiological and anthropometric parameters is present in women diagnosed with PTSD which might be aggravated by the severity and chronicity of the disease.

Complete autonomic blockade reveals nitric oxide contribution to blood pressure regulation in obese Black women

PurposeHypertension is one of the major causes of cardiovascular morbidity and mortality in the USA and disproportionately affects Black women. Endothelial-derived nitric oxide (eNO) substantially regulates blood pressure in humans, and impaired NO-mediated vasodilation has been reported in the Black population. Previous studies using an NO synthase inhibitor, NG-monomethyl-L-arginine (L-NMMA) did not fully determine the NO contribution to blood pressure because of baroreflex buffering. Therefore, in the present study we used trimethaphan, a ganglionic blocker, to inhibit baroreflex buffering and study NO modulation of blood pressure in Black women during L-NMMA infusion.MethodsL-NMMA at doses of 250 μg/kg per minute was infused in combination with trimethaphan at doses of 4 mg/min to eliminate baroreflex mechanisms. Heart rate (HR) was obtained with continuous electrocardiogram monitoring, and continuous blood pressure was measured with the volume clamp method. The increase in systolic blood pressure (SBP) during both infusions was used to estimate the contribution of NO to blood pressure.ResultsTen Black (age range 30–50 years, body mass index [BMI] 30–45 kg/m2), and nine White women (age range 30–50 years, body mass index 30–45 kg/m2) were enrolled in this study. During autonomic blockade, there was no difference in the decrease in SBP between Black and White women (− 20 ± 16.45 vs. − 24 ± 15.49 mm Hg, respectively; P = 0.659). When autonomic blockade was combined with L-NMMA, Black women had a significant increase in SBP compared to White women (54 ± 13.62 vs. 39 ± 09.64 mm Hg, respectively; P = 0.022, respectively).ConclusionAutonomic blood pressure regulation was similar between Black and White women. However, NO contribution to blood pressure was significantly greater in Black women compared to White women.RegistrationClinicalTrials.gov: NCT01122407.

Comparison of isometric handgrip test among pregnant offspring of hypertensive parents and pregnant offspring of non-hypertensive parents.

A family history of hypertension is one of the important risk factors for the development of pregnancy-induced hypertension (PIH). Offspring of hypertensive parents should be screened for PIH. The isometric handgrip (IHG) test is used to assess autonomic function among them. Autonomic function dysregulation can indicate their predisposition to develop PIH later in the course of pregnancy. To compare the IHG among pregnant offspring of hypertensive parents (Group 1) and non-hypertensive parents (Group 2). This is a cross-sectional study done among 100 pregnant women in the second trimester (50 participants in each group). Blood pressure responses to sustained hand grip for 2 minutes of maximum voluntary contraction (MVC) were recorded, immediately at the end of the IHG test and after 5 minutes of the IHG test. Independent t-test and Mann-Whitney U test were used to compare the responses in two groups. There is no statistical difference in basal blood pressure and heart rate between the two groups. Group 1 exhibited a significant increase in systolic blood pressure (SBP) and diastolic blood pressure (DBP) compared to Group 2 immediately after 2 minutes of the IHG test. There is a significant increase in SBP after 5 minutes of the IHG in Group 2. Offspring of hypertensive parents have increased sympathetic reactivity and restoration of the blood pressure is significantly less compared to offspring of normotensive parents, which may predispose them for PIH. IHG can be applied as a convenient tool to screen the population who are at risk of PIH in places like primary health centres or field screenings where IHG is one possible option.

+Acute blood pressure response after Mat Pilates alone and combined with aerobic exercise

The objective of this study was to evaluate the response of systolic blood pressure (SBP) and diastolic blood pressure (DBP) after one session of the Mat Pilates Method alone (traditional) - (MPA) and a second session of the Mat Pilates Method combined with an aerobic exercise (MP + STEP). The sample consisted of 10 adults, of both sexes, Pilates practitioners. Two MP sessions were performed, using 21 original exercises of the method. Blood pressure (BP) was measured before the beginning of the sessions, after 10 min of rest, immediately after the sessions, and 5 min after the end of the sessions. Statistical analyses were performed using generalized estimating equations, α: 5%. In both sessions, SBP (mmHg) increased immediately after (p < 0.001) and returned to baseline values 5 min post-session (p = 0.181) (MPA-rest: 113.90 ± 3.22, immediately after: 120.70 ± 3.57.5; 5 min after: 117.20 ± 2.12; MP + STEP: rest: 112.80 ± 3.03, immediately after: 119.00 ± 3.00, 5 min after: 114.90 ± 2.09). DBP (mmHg) showed a reduction in both sessions immediately (p = 0.001) and 5 min after the sessions (p = 0.008) (MPA - rest: 71.00 ± 2.98; immediately after: 67.00 ± 3 0.03; 5 min after: 67.70 ± 2.31; MP + STEP – rest: 74.90 ± 2.10, immediately after: 67.10 ± 2.63; 5 min after: 70.00 ± 2.23). It is concluded that, regardless of the association with aerobic exercise, the Mat Pilates method can be performed without significant increases in SBP and with a reduction in DBP.

Acute Intake of Fructose Increases Arterial Pressure in Humans: A Meta-Analysis and Systematic Review.

Hypertension is a major cardiac risk factor. Higher blood pressures are becoming more prevalent due to changing dietary habits. Here, we evaluated the impact on blood pressure in human subjects after acutely ingesting fructose using meta-analysis. A total of 89 studies were collected from four different electronic databases from 1 January 2008 to 1 August 2023. Of these studies, 10 were selected that fulfilled all the criteria for this meta-analysis. Heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial blood pressure (MAP), and blood glucose level were analyzed using the Cohen's d analysis or standardized mean difference at a confidence interval (CI) of 95%. The SBP, DBP, and MAP showed medium effect size; HR and glucose level displayed small effect size. The standardized mean difference of normal diet groups and fructose diet groups showed a significant increase in SBP (p = 0.04, REM = 2.30), and DBP (p = 0.03, REM = 1.48) with heterogeneity of 57% and 62%, respectively. Acute fructose ingestion contributes to an increase in arterial pressure in humans. The different parameters of arterial pressure in humans correlated with each other. These findings support further rigorous investigation, retrospective of necessity, into the effect of chronic dietary of fructose in humans in order to better understand the impact on long term arterial pressure.

Angiotensin II-stimulated proximal nephron superoxide production and fructose-induced salt-sensitive hypertension.

Angiotensin II (ANG II) increases proximal tubule superoxide (O2-) production more in rats fed a 20% fructose normal-salt diet compared with rats fed a 20% glucose normal-salt diet. A 20% fructose high-salt diet (FHS) increases systolic blood pressure (SBP), whereas a 20% glucose high-salt diet (GHS) does not. However, it is unclear whether FHS enhances ANG II-induced oxidative stress in proximal tubules and whether this contributes to increases in blood pressure in this model. We hypothesized that FHS augments the ability of ANG II to stimulate O2- production by proximal tubules, and this contributes to fructose-induced salt-sensitive hypertension. We measured SBP in male Sprague-Dawley rats fed FHS and GHS and determined the effects of 3 mM tempol and 50 mg/kg losartan for 7 days. We then measured basal and ANG II-stimulated (3.7 × 10-8 M) O2- production by proximal tubule suspensions and the role of protein kinase C. FHS increased SBP by 27 ± 5 mmHg (n = 6, P < 0.006) but GHS did not. Rats fed FHS + tempol and GHS + tempol showed no significant increases in SBP. ANG II increased O2- production by 11 ± 1 relative light units/µg protein/s in proximal tubules from FHS-fed rats (n = 6, P < 0.05) but not in tubules from rats fed GHS. ANG II did not significantly stimulate O2- production by proximal tubules from rats fed FHS + tempol or FHS + losartan. The protein kinase C inhibitor Gö6976 blunted ANG II-stimulated O2- production. In conclusion, FHS enhances the sensitivity of proximal tubule O2- production to ANG II, and this contributes to fructose-induced salt-sensitive hypertension.NEW & NOTEWORTHY A diet containing amounts of fructose consumed by 17 million Americans causes salt-sensitive hypertension. Oxidative stress is an initiating cause of this model of fructose-induced salt-sensitive hypertension increasing blood pressure. This salt-sensitive hypertension is prevented by losartan and thus is angiotensin II (ANG II) dependent. Fructose-induced salt-sensitive hypertension depends on ANG II stimulating oxidative stress in the proximal tubule. A fructose/high-salt diet augments the ability of ANG II to stimulate proximal tubule O2- via protein kinase C.

A pilot study: Exploring the influence of COVID-19 on cardiovascular physiology and retinal microcirculation

BackgroundThe severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) affects the cardiovascular system. The current study investigated changes in heart rate (HR), blood pressure (BP), pulse wave velocity (PWV), and microcirculation in patients recovering from Coronavirus disease 2019 (COVID-19) infection. MethodologyOut of 43 initially contacted COVID-19 patients, 35 (30 males, 5 females; age: 60 ± 10 years; and body mass index (BMI): 31.8 ± 4.9) participated in this study. Participants were seen on two occasions after hospital discharge; the baseline measurements were collected, either on the day of hospital discharge if a negative PCR test was obtained, or on the 10th day after hospitalization if the PCR test was positive. The second measurements were done 60 days after hospitalization. The vascular measurements were performed using the VICORDER® device and a retinal blood vessel image analysis. ResultsA significant increase in systolic BP (SBP) (from 142 mmHg, SD: 15, to 150 mmHg, SD: 19, p = 0.041), reduction in HR (from 76 bpm, SD: 15, to 69 bpm, SD: 11, p = 0.001), and narrower central retinal vein equivalent (CRVE) (from 240.94 μm, SD: 16.05, to 198.05 μm, SD: 17.36, p = 0.013) were found. Furthermore, the trends of increasing PWV (from 11 m/s, SD: 3, to 12 m/s, SD: 3, p = 0.095) and decreasing CRAE (from 138.87 μm, SD: 12.19, to 136.77 μm, SD: 13.19, p = 0.068) were recorded. ConclusionThe present study investigated cardiovascular changes following COVID-19 infection at two-time points after hospital discharge (baseline measurements and 60 days post-hospitalization). Significant changes were found in systolic blood pressure, heart rate, and microvasculature indicating that vascular adaptations may be ongoing even weeks after hospitalization from COVID-19 infection. Future studies could involve conducting additional interim assessments during the active infection and post-infection periods.

Longitudinal changes in blood pressure and fasting plasma glucose among 5,398 primary care patients with concomitant hypertension and diabetes: Anobservational study and implications for community-based cardiovascular prevention.

To assess longitudinal changes in blood pressure (BP) and fasting plasma glucose (FPG) in primary care patients with concomitant hypertension and type 2 diabetes mellitus (T2DM), and to explore factors associated with patients' inability to improve BP and FPG at follow-up. We constructed a closed cohort in the context of the national basic public health (BPH) service provision in an urbanised township in southern China. Primary care patients who had concomitant hypertension and T2DM were retrospectively followed up from 2016 to 2019. Data were retrieved electronically from the computerised BPH platform. Patient-level risk factors were explored using multivariable logistic regression analysis. We included 5,398 patients (mean age 66 years; range 28.9 to 96.1 years). At baseline, almost half [48.3% (2,608/5,398)] of patients had uncontrolled BP or FPG. During follow-up, more than one-fourth [27.2% (1,467/5,398)] of patients had no improvement in both BP and FPG. Among all patients, we observed significant increases in systolic BP [2.31 mmHg, 95% confidence interval (CI): 2.04 to 2.59, p < 0.001], diastolic BP (0.73 mmHg, 0.54 to 0.92, p < 0.001), and FPG (0.12 mmol/l, 0.09 to 0.15, p < 0.001) at follow-up compared to baseline. In addition to changes in body mass index [adjusted odds ratio (aOR)=1.045, 1.003 to 1.089, p = 0.037], poor adherence to lifestyle advice (aOR = 1.548, 1.356 to 1.766, p < 0.001), and unwillingness to actively enrol in health-care plans managed by the family doctor team (aOR = 1.379, 1.128 to 1.685, p = 0.001) were factors associated with no improvement in BP and FPG at follow-up. A suboptimal control of BP and FPG remains an ongoing challenge to primary care patients with concomitant hypertension and T2DM in real-world community settings. Tailored actions aiming to improve patients' adherence to healthy lifestyles, expand the delivery of team-based care, and encourage weight control should be incorporated into routine healthcare planning for community-based cardiovascular prevention.

PS-B06-9: SINGLE-CELL TRANSCRIPTOMIC PROFILING OF AORTIC B CELLS DURING EXPERIMENTAL HYPERTENSION

Objective: Inflammation and immunity are known to strongly influence aortic fibrosis leading to stiffening and remodelling. We have shown that genetic and pharmacological ablation of B cells affords protection from the development of aortic stiffening and remodelling associated with hypertension. Whether this protective phenotype is due to systemic effects such as reduced antibody secretion, or local B cell effector functions within the aorta remains unclear. Using single-cell transcriptomics, this study aimed to characterise the B cell populations present in the mouse aorta and identify phenotypes/effector functions which may drive inflammation and aortic remodelling. Design and Methods: Hypertension was induced in 12-week-old C57BL6/J mice by infusion of angiotensin II (0.7 mg/kg/day; s.c.) for 28-days via osmotic minipumps. Normotensive mice received vehicle infusion (0.5% NaCl, 0.1% acetic acid). Weekly systolic blood pressure (SBP) measurements were acquired by tail-cuff plethysmography. High-resolution ultrasound imaging was used for pulse wave velocity (PWV) measurements on day 28. Thoracic and abdominal aortas were then isolated and digested for single-cell transcriptomic analyses. Aortic suspensions were stained with Calcein Blue and Vybrant Ruby to sort for metabolically active, nucleated cells. RNA libraries were generated using the 10x Chromium platform. Results and Conclusions: Angiotensin II caused significant increases in SBPs (∼180 mmHg) compared to vehicle treated mice (∼120 mmHg). Hypertensive (HT) mice had increased aortic PWV (∼4 m/s) compared to normotensive (NT) mice (∼1 m/s). Single-cell transcriptomic analyses revealed a near 2-fold increase in B cells present in the aorta of hypertensive mice. Leiden-based community detection identified 7 clusters within the aortic B cell population, including pro-B cells, pre-BCR-independent B cells, transitional B cell populations, B1 and B2 B cells, as well as antibody secreting cells. A greater number of B2 B cells was observed in the hypertensive aorta (58% HT vs 36% NT), without an observable increase in B1 B cell numbers. Gene ontology (GO) analysis of aortic B2 B cells from angiotensin II-treated mice revealed an upregulation in biological processes associated with B cell proliferation (GO:0042100), B cell activation (GO:0042113) and leukocyte differentiation (GO:0002521) compared to vehicle controls. Interestingly, the majority of antibody secreting cells in the aorta appear to be derived from B1 B cells in both vehicle (∼82%) and angiotensin II-treated mice (∼96%). In summary, hypertension is associated with a divergent aortic B cell transcriptome reflective of an augmented immune response, with observable shifts in composition which may be associated with inflammation and aortic remodelling.

Evaluation of Cardiovascular Effects of Carvacrol in a D-(+)-Galactose-Induced aging Model

Aim: To evaluate the cardiovascular effect of carvacrol treatment in a D(+)galactose accelerated aging model, investigating effects on vascular reactivity, oxidative stress, and systolic blood pressure (SBP).&#x0D; Methodology: Eight-week-old male Wistar rats (Rattus norvegicus) were used for oral treatment for eight weeks. Organ baths were used for vascular reactivity studies (FEN, ACh, and NPS), fluorescence microscopy to detect reactive oxygen species (ROS, using DHE probe), and Tail-Cuff for systolic blood pressure (SBP) measurements. Non-linear regression was used to create the concentration-response curves. Emax denotes the tissue's maximum response.&#x0D; Results: The aged rats showed a significant increase in fluorescence intensity by the DHE probe compared to the CTL group (CTL=100 ± 3.6%, n=5 and Dgal=167.7 ± 7.9%, n=5, respectively). However, the levels of ROS in the carvacrol-treated groups were significantly attenuated in the Dgal+C50 (138.8 ± 4.5%, n=5) and Dgal+C100 (130.0 ± 5.5%, n=5) groups. The animals of the Dgal group presented hypertension through the significant increase in SBP compared to the CTL group (CTL=135.9 ± 3.9 mmHg, n=6, Dgal=170.9 ± 2.0 mmHg, n=9, respectively). The increased SBP of Dgal rats could be reversed by treatment with carvacrol (Dgal+C50=137.9 ± 2.7 mmHg, n=5, and Dgal+C100=124.6 ± 8.2 mmHg, n=5, respectively. On the other hand, carvacrol was unable to restore the ACh-induced vasorelaxation effect found in CTL (Emax=100.0 ± 3.9%), Dgal (Emax=84.9 ± 4.4%), Dgal+C50 (Emax=84.9 ± 4.4%) and Dgal+C100 (Emax=82.1 ± 6.2 %).&#x0D; Conclusion: Carvacrol shows protective antioxidant effects capable of reducing SBP in aged animals, being an important tool in promoting healthy aging.

The Impact of Obesity on Cardiovascular Fitness in Young Individuals.

BackgroundYoung individuals are often at a higher risk for cardiovascular disease and obesity due to lifestyle changes like less physical activity and a sedentary lifestyle.ObjectiveThe aim of this study is to determine cardiovascular fitness in young individuals and to study the effects of obesity on their cardiovascular fitness.Material and methodsIn this study, 100 young individuals, out of which 50 were individuals with obesity and 50 were controls, including males and females, of the age group 18-25 years were included. Cardiovascular fitness was assessed in them using body mass index (BMI) and waist-to-hip ratio (WHR). Parameters like SBP (systolic blood pressure), DBP (diastolic blood pressure), PR (pulse rate), and HFI (Harvard fitness index) were measured.ResultsThere was no difference found in the PR of the group with obesity compared to the control group (79.020/min ± 8.651 versus 79.42/min ± 6.737; p value = 0.797). However, a significant increase was observed in both SBP and DBP amongst the group with obesity compared to the control group (SBP = 122.72 mmHg ± 12.287 versus 110.92 mmHg ± 11.803; p-value < 0.001, DBP = 81.96 mmHg ± 7.913 versus 73.24 mmHg ± 11.06; p-value < 0.001). There was a significant reduction in HFI in the group with obesity than in the control group (57.44% ± 9.322 versus 80.34% ± 12.594; p-value < 0.001). When we compared males with obesity and females with obesity, we observed a non-significant difference in PR between males with obesity and females with obesity (77.12/min ± 6.02 versus 80.92/min ± 10.44; p-value = 0.122). However, we found a significant increase in SBP in males with obesity compared to females with obesity (127.76 mmHg ± 10.93 versus 117.68 mmHg ± 11.66; p-value < 0.01). A significant decrease in DBP in males with obesity (78.80 mmHg ± 7.55 versus 85.12 mmHg ± 7.07; < 0.01) than in females with obesity was also observed. Along with a non-significant increase in HFI value in males with obesity compared to females with obesity (58.96% ± 8.14 versus 55.92% ± 10.31; p-value = 0.253).ConclusionResults suggest that both male and female young individuals with obesity are at higher risk for developing cardiovascular comorbidities in the future. So, we need to focus on encouraging activities that promote physical fitness.

Abstract 016: Magnesium Deficient Diet-induced Hypertension And Renal DC-specific NLRP3 Inflammasome Activation

Background: Analysis from a 2013-2016 dietary survey by the National Health and Nutrition Examination Survey Several found that less than 50% of Americans consume sufficient magnesium. Multiple studies have identified a link between dietary magnesium and inflammation associated with multiple pathologies including hypertension, chronic kidney disease, and cardiovascular disease. Additionally, magnesium sulfate inhibits NLRP3 inflammasome activation in human macrophages. We have previously shown that activation of the NLRP3 inflammasome is a key component of salt-sensitive hypertension. In this study, we hypothesize that a magnesium-deficient diet could promote NLRP3 inflammasome activation in myeloid cells and systemic hypertension. Materials and Methods: In vivo studies were performed on mice with an SV/129 background given either a normal-magnesium (Norm-Mg 2+ ) diet (0.08%, as magnesium oxide) or low-magnesium (Low-Mg 2+ ) diet (0.01%) for 5 weeks. Systolic blood pressure (SBP) was monitored on a weekly basis by tail-cuff. Results: Mice fed a Low-Mg 2+ diet had a significant increase in SBP compared to the Norm-Mg 2+ diet fed mice (105.8 ± 11.3 to 130.4 ± 7.4 mmHg vs 106.5 ± 9.4 to 121.8 ± 6.5 mmHg, [n=7, p=0.0071, 2 way ANOVA]). Using flow cytometry, we observed an increase in NLRP3 (34.1 ± 2.5 vs 7.4 ± 0.6 % of DCs, [n=5-7, p=0.0025, Mann-Whitney test]) and IL-1β (41.9 ± 6.6 vs 15.86 ± 6.6 % of DCs, [n=5-7, p=0.048, Mann-Whitney test]) expression in renal dendritic cells (DCs) of Low-Mg 2+ mice compared to Norm-Mg 2+ mice. There was a similar increase in IsoLG-adduct formation in renal DCs (8.5 ± 2.0 vs 0.6 ± 0.05 % of DCs, [n=5-7, p=0.0025, Mann-Whitney test). Interestingly, we found no difference in NLRP3 (24.92 ± 5.3 vs 31.54 ± 3.1 % of monocytes, [n=5-7, p=0.1376, Mann-Whitney test]), IL-1β (9.5 ± 4.3 vs 4.6 ± 0.4 % of monocytes, [n=5-7, p=0.7551, Mann-Whitney test]), or IsoLG-adduct formation (29.42 ± 3.6 vs 31.9 ± 3.6 % of monocytes, [n=5-7, p=&lt;0.999, Mann-Whitney test]) in renal monocytes. Conclusions: Our findings suggest a magnesium-deficient diet induces a hypertensive response and activates the NLRP3 inflammasome in renal DCs but not monocytes.

Racial and ethnic differences in blood pressure before and after the 2016 United States general election.

The 2016 U.S. presidential election was a major source of stress among many adults. Psychosocial stress can manifest physiologically in elevated blood pressure (BP). Little is known regarding the association of macro-level sociopolitical events with BP changes at the population-level. This study sought to characterize population-level changes in BP following the 2016 U.S. presidential election. Using 2015-2018 National Health and Nutrition Examination Survey, we included participants aged ≥18 years during the same periods prior to (May to October 2015/2016) and after (May to October 2017/2018) the election. Survey-weighted data were analyzed to compare population-level systolic BP (SBP) and diastolic BP (DBP) pre- and post-election, stratified by race/ethnicity. Sex differences were also investigated. We observed significant increases in SBP among non-Hispanic (NH) Asian participants (+3.4 mmHg; p=.046), but not among other racial/ethnic participants. DBP increased among NH Black participants (+2.3 mmHg; p=.049) and Mexican American participants (+2.9 mmHg; p=.007), but not among other racial/ethnic participants. These changes appeared attributable to differential BP changes by sex. At the population-level, variable changes in BP were observed by race/ethnicity following the 2016 U.S. presidential election, possibly driven by SBP elevations among women.

Raspberry Supplementation Attenuates Blood Pressure and Improves Mesenteric Artery Relaxation in a Nitric Oxide-Independent Mechanism in Angiotensin II-Treated Rats

ObjectivesBerries are rich in polyphenols with strong antioxidant capacity. They have been suggested to exert antihypertensive properties, which may be due to an increase in the levels of endothelial nitric oxide (NO), a potent vasodilator. Thus, the objective of this study was to evaluate the effects of raspberry supplementation on vascular function in angiotensin (Ang) II-treated rats. MethodsEight-week-old Sprague-Dawley rats (n = 8/group) were fed an AIN-93M diet (control, Ang II, and Losartan (LOS; 20 mg/kg/BW) groups) or AIN-93M diet supplemented with 10% w/w freeze-dried raspberry (RB + Ang II) for 7 weeks. At week 5, rats were implanted with subcutaneous osmotic minipumps that delivered 0.9% saline (CON) or Ang II (270 ng/kg BW/min) for an additional 3 weeks. Blood pressure (BP) was measured using tail-cuff plethysmography (n = 7–8/group). First order mesenteric arteries were isolated for vascular relaxation measurements following constriction by U46619 (1 μM) in a wire myograph (n = 3–8/group). Data were found to be normal and analyzed using ANOVA or mixed-model where appropriate. ResultsAng II group showed a significant increase in systolic BP (SBP) (+26.8%, p = 0.002) 2 weeks after implantation as compared to baseline, while CON, RB + Ang II, and LOS groups showed no differences. Final SBP was significantly lower in the CON (–26.4%, p = 0.01), LOS (–28.3%, p = 0.0005), and RB + Ang II (–20.8%, p = 0.03) groups compared to Ang II group. Relaxation was significantly inhibited in the Ang II group in the presence of acetylcholine after incubation with L-NAME (100 μM), a NO synthase inhibitor, when compared to LOS (p = 0.0003) and RB + Ang II (p = 0.0004) groups. Similarly, relaxation in the Ang II group was significantly inhibited after incubation with ODQ (10 μM), a sGC inhibitor, when compared to CON (p = 0.0002), LOS (p = 0.0004), and RB + Ang II (p = 0.0001) group. No significant changes in vessel relaxation were observed after incubation with LY294002 (20 μM), a PI3K inhibitor. ConclusionsWe demonstrate that RB supplementation attenuated Ang II-induced hypertension and abolished the inhibitory effects of L-NAME and ODQ. This suggests that RB may exert its vasodilatory effects in a NO-independent manner. Funding SourcesThe Agriculture and Food Research Initiative (grant no. 2019–67,017-29,257/project accession no. 1,018,642) from the USDA National Institute of Food and Agriculture.

Raspberry Consumption Reduces ACE1 and NADPH Oxidase Expression in the Kidneys of Mice, Mitigating the Hypertensive Effects of a High-Fat, High-Sucrose Diet.

ObjectivesTo determine whether a diet supplemented with raspberry (RB) is effective at reducing high-fat, high-sucrose (HFHS) diet-induced hypertension through alterations in the renin angiotensin system (RAS) in the kidneys. MethodsEight-week-old male C57BL/6 mice were fed an AIN-93M control diet with or without 10% w/w freeze-dried RB for 4 weeks. They were then randomized into three groups: control (CON), HFHS, or RB + HFHS for 24 weeks. Blood pressure (BP) was measured via tail-cuff plethysmography (n = 6–9/group). Mice were then sacrificed and kidneys were collected for analysis (n = 4–6/group). Protein expression of the pro-oxidant enzymes, NADPH oxidase (NOX) 1 and 4, and RAS components, angiotensin II receptor type 1 (AT1R) and angiotensin converting enzyme 1 (ACE1), were assessed by western blot. Data were analyzed by ANOVA or Kruskal-Wallis, dependent on normality, followed by Dunnett’s post-hoc analysis for multiple comparisons. ResultsConsumption of a HFHS diet for 24 weeks led to a significant increase in systolic BP (120.6 ± 6.8 vs. 98.0 ± 7.1 mmHg, p < 0.0001) compared to CON, which was prevented by dietary RB supplementation (98.9 ± 6.3 mmHg, P < 0.0001). In the kidney, a HFHS diet significantly increased the expression of NOX1 (2.20 ± 0.61 vs. 1.00 ± 0.32-fold, p = 0.008) and NOX4 (2.10 ± 0.86 vs. 1.00 ± 0.32-fold, p = 0.01) compared to CON. RB consumption attenuated the expression of NOX1 (1.22 ± 0.69-fold, p = 0.03) and NOX4 (0.72 ± 0.16-fold, p = 0.005) compared to the HFHS. Expression of AT1R in the kidney was significantly increased by HFHS diet consumption (3.19 ± 1.7 vs. 1.00 ± 0.54-fold, p = 0.02) compared to CON. While RB consumption did not significantly decrease AT1R compared to the HFHS group (1.90 ± 0.38-fold, p = 0.1), its expression did not differ significantly from control (p = 0.3). RB consumption did, however, significantly decrease expression of ACE1 in the kidney (0.96 ± 0.25 vs. 0.29 ± 0.16-fold, p = 0.0009) compared to HFHS. ConclusionsOur results suggest the potential for RB to mitigate the hypertensive effects of a HFHS diet by favorably altering the expression of RAS components and markers of oxidative stress in the kidney. Funding SourcesThis work is supported by the Lewis College Foundation and the Agriculture and Food Research Initiative (grant no. 2019–67,017-29,257/project accession no. 1,018,642) from the USDA National Institute of Food and Agriculture.

Effect of Formaldehyde Exposure on Some Cardiovascular Indices among Morticians in Benin City Nigeria

Introduction: The effect of formaldehyde exposure on some indices of cardiovascular function among morticians in Benin City was studied. Materials and Methods: Fifty subjects were recruited for the study which included 10 nonmorticians and 40 morticians. Subjects were divided into five groups A, B, C, D, and E according to their duration (in years) of exposure to formaldehyde with ten subjects in each group. Group A served as the control (nonmorticians), whereas Groups B, C, D, and E served as the test groups with 0–5 years, 6–10 years, 11–20 years, and &gt;20 years exposures, respectively. Anthropometric parameters were measured as well as some cardiovascular indices which include pulse rate, systolic blood pressure (SBP), diastolic blood pressure (DBP), pulse pressure, and mean arterial pressure (MAP). Statistical analysis was done using GraphPad Prism version 5.0. Results were presented as mean ± standard error of the mean analysis of variance was used to compare the means of test and control values, whereas post hoc test was done using Student[FIGURE DASH]Newman[FIGURE DASH]Keuls test and a P &lt; 0.05 was considered as statistically significant. Results: Results showed significant increases in SBP, DBP, and MAP among Group E morticians. Conclusion: It was therefore concluded that prolonged exposure to formaldehyde could affect the cardiovascular health of morticians.

Efficacy of bolus-dose epinephrine to manage hypotension in the prehospital setting.

Hypotension in the Emergency Department (ED) and the prehospital setting has been associated with significant morbidity and mortality. Limited literature exists exploring the utilization of intravenous (IV) bolus-dose epinephrine (BDE) by Emergency Medical Services (EMS). A retrospective review evaluated patients transported to an academic medical center who had received IV BDE by a single urban EMS system from 2016 to 2020. The primary outcome was to assess the influence IV BDE had on systolic blood pressure (SBP). Secondary objectives were to assess changes in heart rate (HR), the impact of dose variability on SBP, and the incidence of severe hypertension (SBP > 220 mmHg). A total of 55 patients who received 96 administrations of IV BDE were included in the analysis. The most common individual dose was 10 μg (76.0%) and 45.5% received multiple doses. The median weight-based dose of BDE was 0.14 μg/kg. A significant increase in SBP (median 14.0 mmHg) was noted among all patients following BDE administration compared with baseline (p < 0.001). No significant difference was found in HR following BDE compared with baseline (p = 0.375). Those that received a BDE dose >10 μg were noted to have a significantly greater rise in SBP than those that received 10 μg (30.0 mmHg vs. 11.0 mmHg; p = 0.022). Similarly, patients that received a dose ≥0.2 μg/kg had a significantly greater increase in SBP compared with those that received <0.2 μg/kg (30.0 mmHg vs. 10.0 mmHg; p = 0.048). There were no incidences of severe hypertension following therapy. The utilization of IV BDE in the prehospital setting for acute hypotension resulted in a significant rise in SBP. A dose-response relationship was noted both in terms of a flat-based dose and a weight-based dose, with higher doses yielding a greater change in SBP. Additional investigations are necessary to further explore the most appropriate dose of this agent in this setting and its influence, if any, on clinical outcomes.

Hemodynamic Effect of Resuscitative Endovascular Balloon Occlusion of the Aorta in Hemodynamic Instability Secondary to Acute Cardiac Tamponade in a Porcine Model.

The pre-hospital use of Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) is increasing, although it remains controversial, in part because of suggested contraindications such as acute cardiac tamponade (ACT). As both the pre-hospital and in-hospital use of REBOA might potentially occur with concurrent ACT, knowledge of the hemodynamic effect of REBOA in this setting is crucial. This study, therefore, aimed at investigating the physiological effects of REBOA in hemodynamic instability secondary to ACT in a porcine model. We hypothesize that REBOA can temporarily increase systemic blood pressure and carotid blood flow, and prolong survival, in hemodynamic shock caused by ACT. Fourteen pigs (24-38 kg) underwent ACT, through true cardiac injury and hemorrhage into the pericardial space, and were allowed to hemodynamically deteriorate. At a systolic blood pressure (SBP) of 50 mm Hg (SBP50) they were randomized to total occlusion REBOA in zone 1 or to a control group. Survival, hemodynamic parameters, carotid blood flow (CBF), femoral blood flow (FBF), cardiac output (CO), end-tidal CO2, and arterial blood gas parameters were analyzed. REBOA intervention was associated with a significant increase in SBP (50 mm Hg to 74 mm Hg, P = 0.016) and CBF (110 mL/min to 195 mL/min, P = 0.031), with no change in CO, compared to the control group. At 20 min after SBP50, the survival rate in the intervention group was 86% and in the control group 14%, with time to death being significantly longer in the intervention group. This randomized animal study demonstrates that REBOA can help provide hemodynamic stabilization and prolong survival in hemodynamic shock provoked by ACT. It is important to stress that our study does not change the fact that urgent pericardiocentesis or cardiac surgery is, and should remain, the standard optimal treatment for ACT.Level of evidence: Prospective, randomized, experimental animal study. Basic science study, therapeutic.