Constriction Of Blood Vessels Research Articles

Observation of the action of ichthyol in women's practice

The author used ichthyol in 278 cases, using it not only in gynecological cases, but for the treatment of this organism in general, guided by the following pharmacological data: being the double salts of ichthyosulfinic sodium sodium with ammonium, zinc, lithium and containing mainly sulfur, greedily combines with water, what is the effect of reduction and drying; and the ability to irritate tissues less than other drugs has already been proven Unn, They constrict blood vessels, absorb the liquid parts of inflammatory products, (bloodless tissues, and quickly destroy their swelling).

Lactate and nitric oxide regulation in male Wistar rats exposed to lead

Lead is an environmental toxicant that has been implicated in the etiology of many illnesses. It has been reported to cause the constriction of blood vessels. However, it’s not clear if this effect is exhibited by regulating the level of vasodilator substances in the blood. This study was designed to investigate the effects of lead exposure on lactate and nitric oxide regulation in male Wistar rats. Eighty (80) Wistar rats were divided into two groups of 40 rats each. Group 1 served as control and was given water while group 2 was exposed to lead acetate (1000 mg/L) for forty days. Five rats were sacrificed from each group (n=5) on days 5, 10, 15, 20, 25, 30, 35 and 40. Lactate concentration was determined using spectrophotometry procedure. Nitrite concentration was estimated by using the Griess reaction. Lactate concentration increased significantly (p< 0.05) in lead acetate group compared to control in all the durations of exposure. Nitrite concentration decreased significantly (p< 0.05) in lead acetate group compared to control at days 25, 30, 35 and 40 of exposure to lead. The vasodilative effect of lactate may have been suppressed possibly by the overriding vasoconstrictive effect of lead. Lead may have also inhibited the signaling pathways responsible for the production of nitric oxide and relaxation of vascular smooth muscle which enhances blood flow and blood pressure control.

VAV3 rs7528153 and VAV3-AS1 rs1185222 polymorphisms are associated with an increased risk of developing hypertension

The aetiology of essential hypertension is complex and involves both environmental and genetic factors. Approximately 30% of the inter-individual variability in blood pressure is genetically determined. It has been shown that numerous vasoconstrictors stimulate RhoA in local populations of vascular SMCs that, in turn, promote localised constriction of arterial blood vessels and elevations in blood pressure. The VAV3 gene encodes for VAV3 protein, a Rho GEF factor. VAV3-AS1 gene, a lncRNA, may regulate VAV3 expression. We performed an observational prospective case-control study, including patients attending in the Vascular Risk Unit from the University Hospital Salamanca for 6 months. A replication study was performed with data from The Kaiser Permanent database of the University of California. The results suggest that T allele of the VAV3 rs7528153 and G allele of the VAV3-AS1 rs11185222 polymorphisms are associated with an increased risk of developing hypertension. We hypothesise that these polymorphisms could modify blood pressure, likely through a modification in the Rho/Rac pathway. Our results suggest that those polymorphisms could be useful genetic markers of susceptibility to suffering hypertension.

Angiotensin-Converting-Enzyme Inhibitors Protect Against Uterine Fibroids [08B

INTRODUCTION: Uterine leiomyomas are the most common benign pelvic tumor in women. Angiotensin-converting-enzyme inhibitors (ACEi) are a drug-class used for the treatment of hypertension and work by inhibiting the production of angiotensin, an enzyme that promotes blood vessel constriction and tumorigenesis. Angiotensin receptors are expressed in human uterine fibroids and blocking these receptors in animal models has been shown to inhibit leiomyoma cell proliferation. The aim of this population-based study is to examine the association between ACEi use and risk of uterine fibroids and fibroid-related symptoms. METHODS: This nested-case control study included women (n=5,563,980) aged 19–64 with a diagnosis of hypertension during 2010. Cases (n=1,390,995) with a uterine fibroid diagnosis were matched to controls (n=4,172,985) at a 1:3 ratio by age. A conditional logistic regression model was used to calculate odds ratios (OR) and confidence intervals (CI) correlating ACEi use with the risk of uterine fibroid development. An unconditional logistic regression was used to relate ACEi use with fibroid-related symptoms. RESULTS: The cohort with previous exposure to ACEi demonstrated a decreased risk of uterine fibroid development (OR 0.86, 95% CI 0.85–0.86) compared to those who were not exposed to ACEi. ACEi use was associated with lowered risk of experiencing fibroid-related symptoms like anemia (OR 0.88, 95% CI 0.88–0.89) and pelvic pain (OR 0.90, 95% CI 0.90–0.91). CONCLUSION: Angiotensin-converting-enzyme inhibitor use is associated with a reduced risk of the development of uterine fibroids and fibroid-related symptoms. Our findings demonstrate a potential novel therapy for uterine fibroids.

PENYAKIT HIPERTENSI PADA LANSIA DI DESA HURABA KECAMATAN BATANG ANGKOLA KABUPATEN TAPANULI SELATAN TAHUN 2020

Hypertension can be defined as persistent blood pressure where the systolic pressure is above 140 mmHg and the diastolic pressure is above 90 mmHg. Hypertension is said to be mild if the diastolic pressure is between 95-104 mmHg, moderate hypertension if the diastolic pressure is between 105 and 114 mmHg and severe hypertension when the diastolic pressure is 115 mmHg or more. This division is based on an increase in diastolic pressure because it is considered more serious than an increase in systolic (Padila, 2013). The wrong diet is one of the risk factors that increase hypertension. Junk food is a major contributor to hypertension. Excess fat intake causes fat levels in the body to increase, especially cholesterol which causes weight gain so that blood volume experiences a greater increase in pressure. Excess sodium intake will increase extracellular causing blood volume which has an impact on the onset of hypertension. Lack of consuming food sources containing potassium causes the amount of sodium to accumulate and will increase the risk of hypertension (Junaedi, et al. 2013).Benteng Huraba Village is one of the villages in Batang Angkola sub-district, South Tapanuli district which has a fairly large number of elderly, the purpose of community service is to provide information to the community, especially the elderly regarding knowledge about hypertension disease counseling in the elderly in Huraba village, Batang Angkola district South Tapanuli with 42 elderly people. The results of this community service were enthusiastically received by the elderly in Benteng Huraba Village as seen from the many elderly who asked about information about the dangers of hypertension and its causes, where the habit of drinking coffee increases the risk of hypertension, but it depends on the frequency of daily consumption. Drinking coffee and smoking can stimulate constriction of blood vessels so that it can increase blood pressure.Knowledge about the importance of knowing the dangers of hypertension is very useful for the community, especially the elderly in Huraba Village, Batang Angkola District, with this knowledge, it is hoped that it will change the wrong lifestyle, change unhealthy habits and family members are expected to be able to maintain diet so that the elderly live healthier.

Effect of stenosis shape on the sound emitted from a constricted blood vessel.

Effect of stenosis shape on the post-stenotic pressure fluctuations and the sound emitted from a constricted blood vessel is studied numerically. Large eddy simulations are performed using OpenFOAM under pulsatile flow conditions with a non-Newtonian fluid model. Findings indicate that the high slope at the stenosis entrance and overlap of more than one stenosis shorten the length of the flow jet, trigger turbulence, and increase vortical activity, turbulent kinetic energy, and magnitude of pressure fluctuations at the post-stenotic region. Also, these morphological parameters strengthen the audible signal especially in the systolic phase of the pulsatile flow. On the other hand, asymmetry of the stenosis creates an opposite effect. Based on the wall pressure data, it is shown that the stenosis shape affects the intensity and the pattern of the murmurs generated. Stenosis shape is found to be an essential factor for the acoustic-based non-invasive diagnosis of stenosis. Graphical abstract Wall pressure content of the elliptic stenosis shape.

Risks from Breathing Elevated Oxygen.

INTRODUCTION: Effects of breathing gas with elevated oxygen partial pressure (Po₂) and/or elevated inspired oxygen fraction (FIo₂) at sea level or higher is discussed. High FIo₂ is associated with absorption problems in the lungs, middle ear, and paranasal sinuses, particularly if FIo₂ > 80% and small airways, Eustachian tubes, or sinus passages are blocked. Absorption becomes faster as cabin altitude increases. Pulmonary oxygen toxicity and direct oxidative injuries, related to elevated Po₂, are improbable in flight; no pulmonary oxygen toxicity has been found when Po₂ < 55 kPa [418 Torr; 100% O₂ higher than 15,000 ft (4570 m)]. Symptoms with Po₂ of 75 kPa [520 Torr; 100% O₂ at 10,000 ft (3050 m)] were reported after 24 h and the earliest signs at Po₂ of 100 kPa (760 Torr, 100% O₂ at sea level) occurred after 6 h. However, treatment for decompression sickness entails a risk of pulmonary oxygen toxicity. Elevated Po₂ also constricts blood vessels, changes blood pressure control, and reduces the response to low blood sugar. With healthy lungs, gas transport and oxygen delivery are not improved by increasing Po₂. Near zero humidity of the breathing gas in which oxygen is delivered may predispose susceptible individuals to bronchoconstriction.Shykoff BE, Lee RL. Risks from breathing elevated oxygen. Aerosp Med Hum Perform. 2019; 90(12):1041-1049.

Personal Mastery Model on the Ability to Self Care in the Primary Hypertension

Elderly was someone who has reached 60 years and over. One of the factors that affect the physical condition of the elderly is the cardiovascular problem that most suffered by the elderly. As a result of the aging process the blood vessels become stiff and cause the left ventricular wall to decrease its elasticity, resulting in a progressive increase in pressure progressively. Increased peripheral vascular resistance due to vasoconstriction or constriction of blood vessels is a factor in the occurrence of hypertension. Physically someone who has entered the old age all the function of the organs will decrease, so it will affect the daily activities of the elderly. A person who enters the elderly and suffers from hypertension will experience a decrease in physical function so that it will disturb the elderly in meeting their daily needs (Activity Daily Living). The purpose of this research was to develop the elderly Personal Mastery approach model on the ability of elderly self care with primary hypertension. This type of research uses a cross sectional approach. This research was conducted in community health center of Jember Regency in 2017. This research uses rule of thumb, so it needs sample of 100-155 respondents or 5-10 times indicators (observed variables) in the model used is 150 elderly. Instrument collected data with questioner. Analized data used PLS.The result of this research showed that elderly factor, nurse factor, family factor, Integrated Coaching Post service factor, personal mastery, self efficacy, self care agency have an effect on the improvement of self-care ability in Elderly with Primary Hypertension.

A robust diving response in the laboratory mouse.

The diving response is a coordinated physiological response to submersion under water and has been documented amongst all mammals tested to date. The physiological response consists of three primary reflexes: an immediate bradycardia, apnea, and selective constriction of peripheral blood vessels. We hypothesized that mice would exhibit a diving response upon voluntary submersion into water typically seen in other mammals. In this study, telemeters that measure arterial pressure were implanted into male and female C57Bl/6J mice. These mice were trained to voluntarily dive underwater for a distance of 40cm over a 4-6s period. Just before the dive, the interbeat interval (IBI) was 87 ± 6ms (mean ± SD) and diastolic pressure was 99 ± 14mmHg. Underwater submersion caused (1) a dramatic bradycardia immediately at the onset of each dive, as IBI increased to 458 ± 104ms, and (2) a large drop in diastolic pressure, to 56 ± 16mmHg despite the elevation in peripheral resistance. Mice experienced a short bout (~ 2s) of hypertension (diastolic pressure rose to 131 ± 17mmHg) upon emergence. The bradycardia and hypotension appeared to be vagally mediated, since both these responses were blocked with atropine pre-treatment. These data demonstrate that the mouse exhibits a robust diving response upon voluntary submersion into water.

Neuropeptide S promotes wakefulness through the inhibition of sleep-promoting ventrolateral preoptic nucleus neurons.

The regulation of sleep-wake cycles is crucial for the brain's health and cognitive skills. Among the various substances known to control behavioral states, intraventricular injection of neuropeptide S (NPS) has already been shown to promote wakefulness. However, the NPS signaling pathway remains elusive. In this study, we characterized the effects of NPS in the ventrolateral preoptic nucleus (VLPO) of the hypothalamus, one of the major brain structures regulating non-rapid eye movement (NREM) sleep. We combined polysomnographic recordings, vascular reactivity, and patch-clamp recordings in mice VLPO to determine the NPS mode of action. We demonstrated that a local infusion of NPS bilaterally into the anterior hypothalamus (which includes the VLPO) significantly increases awakening and specifically decreases NREM sleep. Furthermore, we established that NPS application on acute brain slices induces strong and reversible tetrodotoxin (TTX)-sensitive constriction of blood vessels in the VLPO. This effect strongly suggests that the local neuronal network is downregulated in the presence of NPS. At the cellular level, we revealed by electrophysiological recordings and in situ hybridization that NPSR mRNAs are only expressed by non-Gal local GABAergic neurons, which are depolarized by the application of NPS. Simultaneously, we showed that NPS hyperpolarizes sleep-promoting neurons, which is associated with an increased frequency in their spontaneous IPSC inputs. Altogether, our data reveal that NPS controls local neuronal activity in the VLPO. Following the depolarization of local GABAergic neurons, NPS indirectly provokes feed-forward inhibition onto sleep-promoting neurons, which translates into a decrease in NREM sleep to favor arousal.

Feasability of Introducing a Thioether Ring in Vasopressin by nisBTC Co-expression in Lactococcus lactis.

Introducing one or more intramolecular thioether bridges in a peptide provides a promising approach to create more stable molecules with improved pharmacodynamic properties and especially to protect peptides against proteolytic degradation. Lanthipeptides are compounds that naturally possess thioether bonds in their structure. The model lanthipeptide, nisin, is produced by Lactococcus lactis as a core peptide fused to a leader peptide. The modification machinery responsible for nisin production, including the Ser/Thr-dehydratase NisB and the cyclase NisC, can be applied for introducing a thioether bridge into peptides fused to the nisin leader peptide, e.g., to replace a disulfide bond. Vasopressin plays a key role in water homeostasis in the human body and helps to constrict blood vessels. There are two cysteine residues in the structure of wild type vasopressin, which form a disulfide bridge in the mature peptide. Here, we show it is possible to direct the biosynthesis of vasopressin variants in such a way that the disulfide bridge is replaced by a thioether bridge using the nisin modification machinery NisBTC, albeit at low efficiency. Vasopressin mutants were fused either to the nisin leader peptide directly (Type A), after the first three rings of nisin (Type B/C), or after full nisin (Type D). The type B strategy was optimal for expression. LC-MS/MS data verified the formation of a thioether bridge, which provides proof of principle for this modification in vasopressin. This is a first step prior to the necessary increase of the production yield and further purification of these peptides to finally test their biological activity in tissue and animal models.

Pengaruh Suplementasi Zinc terhadap Waktu Penyembuhan Luka Perineum pada Ibu Nifas

Zinc is a major mineral that the body needs during wound healing. Zinc supplementationhas been widely used as a major component for burns, diaperash due to lessions and other conditions. Perineal wound healing period in the normal puerperal women are 6-7 days. The purpose of this study was to determine the effect of Zinc supplementation on wound healing time of the perineum in the region Arjasa Public Health Center in 2015. The research method uses quasie experimental design with the design of the control group post test only. Its population is experiencing post partum mothers spontaneous rupture in the work area as much as 28 post partum mothers in Arjasa Public Health Center. Sampling was done by accidental sampling technique. The sample consisted of 26 post partum women who experienced spontaneous rupture. Of this sample there are 23 postpartum women were given supplements of Zinc and 23 postpartum women were not given zinc supplements. Results of data analysis using independent test two sample t-test obtained uncorrelated t count is greater thant t table (5.377&gt;2.063), meaning that Ho is rejected. This shows there are influence of Zinc supplementation on perineal wound healing time in postpartum mother. Based on the results of this study, Zinc was instrumental in the proliferatife phase constriction of blood vessels and accelerate the formation of new networks of fibrin fibers that time faster wound healing. Keywords : Zinc supplementation, perineal wound healing time

In Silico Analysis of the Phenylephrine from the Sand Crab (Emerita asiatica) for its Antimicrobial Activities

Aim: The present investigation gives a detailed report on the analysis of the bioactive compound isolated from the sand crab Emerita asiatica is having better relation with vasoconstriction. Methods: The sand crab Emerita asiatica were collected from Thiruvidandhai beach located on the Kanchipuram District, Tamil Nadu, India, 41 K.M away from Chennai, on the East Coast Road route to Mahabalipuram. Sand crabs were collected by hand picking method. From the muscle mass of the Crab the organic compound was isolated by GC-MS analysis. Molecular docking was also performed to identify the protein ligand responsible for the constriction of blood vessels. Results: The isolated bioactive compound was identified as phenylephrine, an a1 adrenergic receptor which has the potential to lead the molecule for the vasoconstriction. In vitro studies of antibacterial activities clearly indicated that the different concentrations of phenylephrine have the antibacterial activity against the bacteria such as Klebsiella pneumoniae and Staphylococcus aureus. Summary: The present investigation would give latest information on the isolation of bioactive compound for the production of pharmaceutical drugs from marine organisms. These results will be decisive factor for determining a lead bioactive compound for further drug discovery process for the vasoconstriction.

Beta-Arrestin1 Prevents Preeclampsia by Downregulation of Mechanosensitive AT1-B2 Receptor Heteromers

Preeclampsia is the most frequent pregnancy-related complication worldwide with no cure. While a number of molecular features have emerged, the underlying causal mechanisms behind the disorder remain obscure. Here, we find that increased complex formation between angiotensin II AT1 and bradykinin B2, two G protein-coupled receptors with opposing effects on blood vessel constriction, triggers symptoms of preeclampsia in pregnant mice. Aberrant heteromerization of AT1-B2 led to exaggerated calcium signaling and high vascular smooth muscle mechanosensitivity, which could explain the onset of preeclampsia symptoms at late-stage pregnancy as mechanical forces increase with fetal mass. AT1-B2 receptor aggregation was inhibited by beta-arrestin-mediated downregulation. Importantly, symptoms of preeclampsia were prevented by transgenic ARRB1 expression or a small-molecule drug. Because AT1-B2 heteromerization was found to occur in human placental biopsies from pregnancies complicated by preeclampsia, specifically targeting AT1-B2 heteromerization and its downstream consequences represents a promising therapeutic approach.

Molecular and biochemical characterization of the bed bug salivary gland cholinesterase as an acetylcholine-sequestering enzyme

The common bed bug, Cimex lectularius, possesses a cholinesterase expressed exclusively in the salivary gland (ClSChE). In this study, we investigated the molecular forms, tissue distribution patterns and biochemical properties of ClSChE and showed that ClSChE exists as a soluble monomeric form or a soluble dimeric form connected by a disulfide bridge. Immunohistochemical analysis confirmed that ClSChE was expressed in the epithelial cells of both the salivary gland and the duct. In addition, the secretion of monomeric ClSChE through the proboscis during feeding was confirmed by western blotting using a ClSChE-specific antibody. To predict the role of ClSChE injected into the tissue of an animal host, we analyzed the extent of hydrolysis of acetylcholine (ACh) by ClSChE by ultra-performance liquid chromatography-tandem mass spectrometry. ClSChE binding to ACh was not clearly resolved in the binding assay format used in this study, probably due to the weak but detectable ACh-hydrolytic activity of ClSChE. Nevertheless, kinetic analysis revealed that ClSChE possesses extremely low Km (high affinity to ACh) and Vmax values. These findings suggest that ClSChE functions virtually as an ACh-sequestering protein by having a very strong affinity to ACh but an extremely long turnover time. Given that ACh regulates a wide variety of host physiologies, we discuss the tentative roles of ClSChE in blood vessel constriction and itch/pain regulation in the host.

Mixed Vascular Nevus Syndrome

Mixed vascular nevus (or nevus vascularis mixtus) represents an admixture of cutaneous vascular malformations of the telangiectatic type and angiospastic spots of nevus anemicus. It can occur as a purely cutaneous trait or as a hallmark of a neurocutaneous phenotype, the so-called mixed vascular nevus syndrome. The latter is characterized by the combination of paired vascular twin nevi and brain abnormalities of the Dyke–Davidoff–Masson type, consisting of crossed cerebral/cerebellar hemiatrophy with hypoplasia of the ipsilateral cerebral vessels, and homolateral hypertrophy of the skull and sinuses (hyperpneumatization) with contralateral hemispheric hypertrophy. In other cases, the paired vascular twin nevi and brain malformations of the Dyke–Davidoff–Masson type occur in association with systemic abnormalities consisting of facial asymmetry, skeletal anomalies, and disorders of autoimmunity. In 2014, Happle proposed to name the syndrome with the eponym Ruggieri–Leech's syndrome after the first two authors who reported (independently) this phenotype in different patients.Pathogenically, this complex phenotype suggests that embryonic pairing and somatic recombination of recessive (didymotic) alleles controlling the balance between constriction (i.e., nevus anemicus) and dilatation (i.e., nevus telangiectaticus) of blood vessels could be the primary event causing the phenomena of cutaneous and brain vascular twin spotting and the paired phenomena of skull hyperpneumatization versus hypertrophy and brain megalencephaly/colpocephaly versus cortical dysplasia.

EFEKTIFITAS KOMPRES HANGAT BASAH DAN KERING TERHADAP NYERI PUNGGUNG BAWAH PADA LANSIA DI WILAYAH KERJA PUSKESMAS TELEN KUTAI TIMUR KALIMANTAN TIMUR

Latar belakang: lansia yang ada di wilayah puskesmas Talen berjumlah 229 orang, terdapat 75 (32,75%) lansia mengalami nyeri punggung bawah. Kompres hangat basah dan kering merupakan salah satu terapi nonfarmakologi dalam mengurangi nyeri namun belum diketahui efektivitas diantara dua terapi tersebut.Tujuan: untuk mengetahui efektivitas antara kompres hangat basah dan kering terhadap nyeri punggung bawah pada lansia di wilayah kerja Puskesmas Telen. Metode penelitian: Quasy eksperiment denganpre and post test without control. Pengambilan sampel dilakukan dengan tehnik Quota Sampling, jumlah sampel sebanyak 32 responden yang dibagi menjadi 2 kelompok. Instrumen Numeric Rating Scale. Uji statistik Mann Whitney. Hasil: Rata-rata penurunan skala nyeri kompres hangat kering 1,94 dan basah 0,19 dengan P value 0,000 ≤ 0,05. Uji beda kompres hangat kering dan basah P value 0,48. Kesimpulan: Tidak ada perbedaan efektivitas kompres hangat basah dan kering terhadap nyeri punggung bawah pada lansia di wilayah kerja Puskesmas Telen. Saran: Untuk peneliti selanjutnya teknik pengambilan sampel menggunakan random agar memberi kesempatan yang sama.Kata kunci : Nyeri Punggung Bawah - Lansia - Kompres hangat basah dan kering

Transient Increase in Sympathetic Constriction of Mesenteric Arteries from High Fat Diet‐Fed Dahl Salt‐sensitive Female Rats

Obesity (BMI ≥ 30) is a risk factor for hypertension. Obesity‐associated hypertension is a risk factor for cardiovascular disease, stroke, type 2 diabetes and kidney failure. Hypertension is less common in premenopausal women compared to age‐matched men. This disparity fades away after the onset of menopause. Increased sympathoexcitation in the neuroeffector junction leads to increase in constriction of blood vessels. Differences in the mechanism/s neurogenic arterial constriction in male and female are not well understood. We hypothesized that sympathetic nerve activity in high fat diet‐induced hypertension is greater in male than female rat mesenteric arteries (MA). Rats were fed either control (C) or high fat (HF) diet beginning at 3 weeks of age, and used at 10, 17 and 24 weeks on diet. Body weight and systolic blood pressure (SBP) were measured weekly. HF males gained more weight than HF females at all time points. SBP was higher in HF rats compared to C rats in both sexes and across all time points. The estrus cycle stage was determined cytologically by vaginal lavage prior to euthanasia. Mesenteric arteries (Inner diameter; male=275–350 μm, female=245–315 μm) were harvested and mounted in a pressure (60 mmHg) myograph and inner diameter was measured continuously. MA contractile responses to electrical field stimulation (30 stimuli at 0.2–30 Hz) and drug applications were measured. Neurogenic constriction of MA from HF females was greater than HF males at 5 and 10 Hz at 10 wks, and at 5–30 Hz at 17 wks. At 24 wks the difference disappears. Constrictions caused by norepinephrine (NE) and ATP were similar in MA from HF male and female rats. Immunostaining for tyrosine hydroxylase (sympathetic nerve marker) and vesicular nucleotide transporter (ATP marker) revealed greater sympathetic nerve intensity in HF male than female rats at 10 and 24 wks. There was also greater intensity in MA from HF males than HF females at 10 and 17 wks. Moreover, HF males have higher NE and ATP nerve density than HF females at 10 and 17 but not for ATP at 24 wks. MA NE levels were similar in male and female rats. Prejunctional α2‐AR and NE transporter functions were not impaired in MA from HF Dahl salt‐sensitive rats. Taken together, despite sex differences in sympathetic nerve density in MA, we detected only transient sex differences in sympathetic neurogenic arterial constrictions. Contrary to our hypothesis, we found that HF females transiently have an upregulation of neurogenic sympathetic activity and this warrants further investigation into the mechanism.Support or Funding InformationResearch supported by PPG NIH Grant P01HL070687This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Angiotensin‐II‐Induced Increase in Blood Pressure in Female and Male Mice

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

Increased permeability of blood vessels after reversible electroporation is facilitated by alterations in endothelial cell-to-cell junctions

Delivery of electric field pulses, i.e. electroporation (EP), to tissues has been shown to have a blood flow modifying effect. Indeed, the diameter of blood vessels exposed to EP is immediately reduced resulting in blood flow abrogation, followed by an increase in vascular permeability. The main cause of the increased permeability remains unknown. The aim of this study was to determine whether the in vivo effects of EP on permeability of blood vessels are linked to the permeabilization of endothelial cells' membrane (EC) and/or disruption of cell-to-cell junctions. We used a dorsal window chamber model in C57Bl/6 mice coupled with multiphoton microscopy and fluorescently labelled antibodies against PECAM-1 (CD31) to visualize endothelial cell-to-cell junctions. Clinically validated EP parameters were used and behavior of cell-to-cell junctions, in combination with leakage of 70 kDa fluorescein isothiocyanate labelled dextran (FD), was followed in time. After EP, a constriction of blood vessels was observed and correlated with the change in the shape of ECs. This was followed by an increase in permeability of blood vessels for 70 kDa FD and a decrease in the volume of labelled cell-to-cell junctions. Both parameters returned to pre-treatment values in 50% of mice. For the remaining 50%, we hypothesize that disruption of cell-to-cell junctions after EP may trigger the platelet activation cascade. Our findings show for the first time in vivo that alterations in cell-to-cell junctions play an important role in the response of blood vessels to EP and explain their efficient permeabilization.