scholarly journals Vascular function and endothelin-1: tipping the balance between vasodilation and vasoconstriction

2017 ◽  
Vol 122 (2) ◽  
pp. 354-360 ◽  
Author(s):  
Steven K. Nishiyama ◽  
Jia Zhao ◽  
D. Walter Wray ◽  
Russell S. Richardson
Keyword(s):  
Vascular Function ◽  
Vascular Endothelial Cells ◽  
Reactive Hyperemia ◽  
Flow Mediated Dilation ◽  
Vascular Endothelial ◽  
Endothelin 1 ◽  
Healthy Humans ◽  
Blood Flow Control ◽  
Potent Vasoconstrictor ◽  
The Impact

Endothelin-1 (ET-1), a potent vasoconstrictor secreted by vascular endothelial cells, has been implicated in the pathophysiology of numerous cardiovascular diseases, yet the direct impact of ET-1 on vascular function remains unclear. Therefore, in seven young (23 ± 1 yr) healthy subjects, we investigated the effect of an intra-arterial infusion of ET-1 on reactive hyperemia (RH) and flow-mediated dilation (FMD) in the popliteal artery following 5 min of suprasystolic cuff occlusion. ET-1 infusion significantly attenuated basal leg blood flow (control: 62 ± 4 ml/min, ET-1: 47 ± 9 ml/min), RH [area-under-curve (AUC); control: 162 ± 15 ml, ET-1: 104 ± 16 ml], and peak RH (control: 572 ± 51 ml/min, ET-1: 412 ± 32 ml/min) ( P < 0.05). Administration of ET-1 also reduced FMD (control: 2.4 ± 0.3%, ET-1: 0.5 ± 0.5%) and FMD normalized for shear rate (control: 10.5 × 10−4 ± 2.0 × 10−4%/s−1, ET-1: 0.9 × 10−4 ± 2.8 ×10−4%/s−1). These findings reveal that elevated levels of ET-1 have a significant impact on vascular function, indicating that studies employing RH and FMD as markers of microvascular function and nitric oxide bioavailability, respectively, should exercise caution, as ET-1 can impact these assessments by tipping the balance between vasodilation and vasoconstriction, in favor of the latter. NEW & NOTEWORTHY Endothelin-1 (ET-1) is recognized as the body’s most potent endogenous vasoconstrictor, but the impact of this peptide on vascular function is not well understood. The present study revealed that the intra-arterial administration of ET-1 impaired both microvascular and conduit vessel function of the leg in young, healthy, humans. Studies employing vascular testing in patient cohorts that experience a disease-related increase in ET-1 should thus exercise caution, as ET-1 clearly impairs vascular function.

scholarly journals Morning impairment in vascular function is unrelated to overnight sleep or the inactivity that accompanies sleep

2018 ◽  
Vol 315 (5) ◽  
pp. R986-R993 ◽  
Author(s):  
Saurabh S. Thosar ◽  
Alec M. Berman ◽  
Maya X. Herzig ◽  
Sally A. Roberts ◽  
Michael R. Lasarev ◽  
...  
Keyword(s):  
Vascular Function ◽  
Physical Inactivity ◽  
Flow Mediated Dilation ◽  
Vascular Endothelial ◽  
Endothelin 1 ◽  
System A ◽  
Before And After ◽  
Markers Of Oxidative Stress ◽  
Dim Light ◽  
Healthy Participants

Adverse cardiovascular events, such as myocardial infarction and sudden cardiac death, occur more frequently in the morning. Prior studies have shown that vascular endothelial function (VEF), a marker of cardiovascular disease, is attenuated during physical inactivity and declines across the night. We sought to determine whether a morning attenuation in VEF is a result of prior sleep or the inactivity that inevitably accompanies sleep. After 1 wk of a rigorously controlled sleep-wake schedule and behaviors, 10 healthy participants completed a randomized crossover protocol in dim light and constant conditions, incorporating a night of 6 h of sleep opportunity and a night of immobility while they were supine and awake. VEF was measured in the dominant brachial artery as flow mediated dilation (FMD) before and after each 6-h trial. To avoid disturbing sleep and posture of the participants, blood was drawn using a 12-ft catheter from an adjoining laboratory room before, during, and after each 6-h trial, and plasma was analyzed for markers of oxidative stress [malondialdehyde adducts (MDA)], and endothelin-1. Contrary to expectation, both nocturnal sleep and nocturnal inactivity significantly increased FMD ( P < 0.05). There was no significant change in MDA or endothelin-1 within and between trials. Contrary to expectations based on prior studies, we found that overnight sleep or the inactivity that accompanies sleep did not result in attenuation in VEF in the morning hours in healthy people. Thus, it is plausible that the endogenous circadian system, a remaining factor not studied here, is responsible for the commonly observed decline in VEF across the night.

scholarly journals Characteristic Analysis of Trigonelline Contained in Raphanus sativus Cv. Sakurajima Daikon and Results from the First Trial Examining Its Vasodilator Properties in Humans

Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1872 ◽  
Author(s):  
Maho Sasaki ◽  
Yuri Nonoshita ◽  
Takashi Kajiya ◽  
Nobuhiko Atsuchi ◽  
Megumi Kido ◽  
...  
Keyword(s):  
Endothelial Function ◽  
Vascular Function ◽  
Raphanus Sativus ◽  
Vascular Endothelial Cells ◽  
Public Health Problem ◽  
Major Public Health Problem ◽  
Flow Mediated Dilation ◽  
Vascular Endothelial ◽  
Vascular Endothelial Function ◽  
Characteristic Analysis

Vascular disease poses a major public health problem worldwide. Trigonelline isolated from Raphanus sativus cv. Sakurajima Daikon (Sakurajima radish) induces nitric oxide production from vascular endothelial cells and enhances vascular function. Here, we investigated the characteristics of trigonelline and its effects on endothelial function after consumption of Sakurajima radish by humans. Our results show that Sakurajima radish contains approximately 60 times more trigonelline than other radishes and squashes. Additionally, no significant differences were observed between varieties of Sakurajima radish, suggesting that any type of Sakurajima radish can be ingested for trigonelline supplementation. The effects of cooking and processing Sakurajima radish were also evaluated, as were the effects of freezing, and changes in osmotic pressure and pH. A first-in-human trial using Sakurajima radish showed that ingestion of 170 g/day of Sakurajima radish for ten days increased blood trigonelline concentrations and significantly improved flow-mediated dilation, which is a measure of vascular endothelial function. Overall, our findings suggest that the trigonelline contained in Sakurajima radish may contribute to improved human vascular endothelial function. Hence, Sakurajima radish may enhance vascular endothelial function as a functional food.

Role of endothelin 1 in regulating rabbit airway contractility

1991 ◽  
Vol 260 (2) ◽  
pp. L75-L82
Author(s):  
M. M. Grunstein ◽  
S. T. Chuang ◽  
C. M. Schramm ◽  
N. A. Pawlowski
Keyword(s):  
Vascular Endothelial Cells ◽  
Maximal Response ◽  
Channel Blockers ◽  
Vascular Endothelial ◽  
Endothelin 1 ◽  
A Value ◽  
Relaxant Response ◽  
Potent Vasoconstrictor ◽  
Dose Dependent

Endothelin 1 (ET-1) is a potent vasoconstrictor peptide recently isolated from vascular endothelial cells. Because its role and mechanisms of action in regulating airway contractility remain to be identified, we examined the contractile effects of ET-1 in isolated rabbit tracheal smooth muscle (TSM) segments. In TSM under passive tension, ET-1 elicited dose-dependent contractions with a mean +/- SE -log 50% of maximal response value of 7.82 +/- 0.13 vs. a value of 5.61 +/- 0.07 -log M for acetylcholine (ACh). In TSM half-maximally contracted with ACh, however, ET-1 exerted dual and opposing contractile effects. Lower doses of ET-1 (less than or equal to 10(-9) M) produced a 74.2 +/- 16.6% decrease in active TSM tension. This relaxant response to ET-1 was associated with an accelerated accumulation of prostaglandin (PG) I2 and PGE2 and was attenuated by cyclooxygenase inhibition with indomethacin (10(-5) M). The combination of indomethacin and removal of the airway epithelium completely inhibited the TSM relaxant response to ET-1. In contrast, higher doses of ET-1 (greater than 10(-9) M) induced airway contractions that were attenuated by the Ca2+ channel blockers nifedipine (10(-5) M) and diltiazem (10(-5) M) and ablated in Ca2(+)-free buffer. Moreover, ET-1-induced TSM contractions were inhibited by the protein kinase C (PK-C) antagonists 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine, and staurosporine.(ABSTRACT TRUNCATED AT 250 WORDS)

Human serum stimulates endothelin-1 synthesis more potently than prostacyclin production by cultured vascular endothelial cells

Life Sciences ◽  
1991 ◽  
Vol 49 (8) ◽  
pp. 603-609 ◽  
Author(s):  
Ari Ristimäki ◽  
Risto Renkonen ◽  
Outi Saijonmaa ◽  
Olavi Ylikorkala ◽  
Lasse Viinikka
Keyword(s):  
Endothelial Cells ◽  
Human Serum ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Endothelin 1 ◽  
Prostacyclin Production

scholarly journals The bone marrow niche components are adversely affected in sepsis

2020 ◽  
Vol 1 (1) ◽  
Author(s):  
Fan Yin ◽  
Han Qian ◽  
Caiwen Duan ◽  
Botao Ning
Keyword(s):  
Bone Marrow ◽  
Vascular Endothelial Cells ◽  
Cecal Ligation ◽  
Treg Cells ◽  
Multiple Organ ◽  
Bone Marrow Niche ◽  
Vascular Endothelial ◽  
Bm Niche ◽  
Cell Components ◽  
The Impact

Abstract Multiple organ dysfunction is an important cause of death in patients with sepsis. Currently, few studies have focused on the impact of sepsis on bone marrow (BM), especially on the cell components of BM niche. In this study, we performed mouse sepsis models by intraperitoneal injection of LPS and cecal ligation and puncture (CLP). The changes of niche major components in the mouse BM among vascular structures, mesenchymal stem cells and Treg cells were observed and analyzed. The results showed that pathological changes in BM was earlier and more prominent than in other organs, and various cell components of the BM niche changed significantly, of which vascular endothelial cells increased transiently with vascular remodeling and the regulatory T cells decreased over a long period of time. These results indicated that the components of the BM niche underwent series of adaptive changes in sepsis.

scholarly journals Immobilized DNA aptamers used as potent attractors for vascular endothelial cell: in vitro study of female rat

2020 ◽  
Vol 40 (1) ◽  
Author(s):  
Jung-Joon Cha ◽  
Hoyeon Lee ◽  
Miyoung Kim ◽  
Juyoung Kang ◽  
Hanlim Song ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Vascular Function ◽  
Therapeutic Potential ◽  
Vascular Endothelial Cells ◽  
Specific Binding ◽  
Vascular Endothelial Cell ◽  
Dna Aptamers ◽  
Female Rat ◽  
Vascular Endothelial

Abstract Vascular endothelial cells are essential to vascular function and maintenance. Dysfunction of these cells can lead to the development of cardiovascular disease or contribute to tumorigenesis. As such, the therapeutic modulation and monitoring of vascular endothelial cells are of significant clinical interest, and several endothelial-specific ligands have been developed for drug delivery and the monitoring of endothelial function. However, the application of these ligands has been limited by their high cost and tendency to induce immune responses, highlighting a need for alternate methods of targeting vascular endothelial cells. In the present study, we explore the therapeutic potential of DNA aptamers. Using cell-SELEX technology, we identified two aptamers with specific binding affinity for vascular endothelial cells and propose that these molecules show potential for use as new ligands for drug and biomarker research concerning vascular endothelial cells.

Aerobic exercise training reduces plasma endothelin-1 concentration in older women

2003 ◽  
Vol 95 (1) ◽  
pp. 336-341 ◽  
Author(s):  
Seiji Maeda ◽  
Takumi Tanabe ◽  
Takashi Miyauchi ◽  
Takeshi Otsuki ◽  
Jun Sugawara ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Exercise Training ◽  
Aerobic Exercise ◽  
Older Women ◽  
Ventilatory Threshold ◽  
Vascular Endothelial Cells ◽  
Aerobic Exercise Training ◽  
Vascular Endothelial ◽  
Middle Aged ◽  
Endothelin 1

Endothelial function deteriorates with aging. On the other hand, exercise training improves the function of vascular endothelial cells. Endothelin-1 (ET-1), which is produced by vascular endothelial cells, has potent constrictor and proliferative activity in vascular smooth muscle cells and, therefore, has been implicated in regulation of vascular tonus and progression of atherosclerosis. We previously reported significantly higher plasma ET-1 concentration in middle-aged than in young humans, and recently we showed that plasma ET-1 concentration was significantly decreased by aerobic exercise training in healthy young humans. We hypothesized that plasma ET-1 concentration increases with age, even in healthy adults, and that lifestyle modification (i.e., exercise) can reduce plasma ET-1 concentration in previously sedentary older adults. We measured plasma ET-1 concentration in healthy young women (21–28 yr old), healthy middle-aged women (31–47 yr old), and healthy older women (61–69 yr old). The plasma level of ET-1 significantly increased with aging (1.02 ± 0.08, 1.33 ± 0.11, and 2.90 ± 0.20 pg/ml in young, middle-aged, and older women, respectively). Thus plasma ET-1 concentration was markedly higher in healthy older women than in healthy young or middle-aged women (by ∼3- and 2-fold, respectively). In healthy older women, we also measured plasma ET-1 concentration after 3 mo of aerobic exercise (cycling on a leg ergometer at 80% of ventilatory threshold for 30 min, 5 days/wk). Regular exercise significantly decreased plasma ET-1 concentration in the healthy older women (2.22 ± 0.16 pg/ml, P < 0.01) and also significantly reduced their blood pressure. The present study suggests that regular aerobic-endurance exercise reduces plasma ET-1 concentration in older humans, and this reduction in plasma ET-1 concentration may have beneficial effects on the cardiovascular system (i.e., prevention of progression of hypertension and/or atherosclerosis by endogenous ET-1).

scholarly journals Meta-analysis of Exercise Training on Vascular Endothelial Function in Cancer Survivors

2018 ◽  
Vol 17 (2) ◽  
pp. 192-199 ◽  
Author(s):  
Rhys I. Beaudry ◽  
Yuanyuan Liang ◽  
Steven T. Boyton ◽  
Wesley J. Tucker ◽  
R. Matthew Brothers ◽  
...  
Keyword(s):  
Exercise Training ◽  
Endothelial Function ◽  
Cancer Survivors ◽  
Vascular Function ◽  
Meta Analysis ◽  
Reactive Hyperemia ◽  
Controlled Trials ◽  
Vascular Endothelial ◽  
Vascular Endothelial Function ◽  
Randomized Controlled

Cancer and cardiovascular disease (CVD) are leading causes of morbidity and mortality in the United States. Vascular endothelial dysfunction, an important contributor in the development of CVD, improves with exercise training in patients with CVD. However, the role of regular exercise to improve vascular function in cancer survivors remains equivocal. We performed a meta-analysis to determine the effect of exercise training on vascular endothelial function in cancer survivors. We searched PubMed (1975 to 2016), EMBASE CINAHL (1937 to 2016), OVID MEDLINE (1948 to 2016), and Cochrane Central Registry of Controlled Trials (1991 to 2016) using search terms: vascular function, endothelial function, flow-mediated dilation [FMD], reactive hyperemia, exercise, and cancer. Studies selected were randomized controlled trials of exercise training on vascular endothelial function in cancer survivors. We calculated pooled effect sizes and performed a meta-analysis. We identified 4 randomized controlled trials (breast cancer, n=2; prostate cancer, n=2) measuring vascular endothelial function by FMD (n=3) or reactive hyperemia index (n=1), including 163 cancer survivors (exercise training, n=82; control, n=81). Aerobic exercise training improved vascular function (n=4 studies; standardized mean difference [95% CI]=0.65 [0.33, 0.96], I2=0%; FMD, weighted mean difference [WMD]=1.28 [0.22, 2.34], I2=23.2%) and peak exercise oxygen uptake (3 trials; WMD [95% CI]=2.22 [0.83, 3.61] mL/kg/min; I2=0%). Our findings indicate that exercise training improves vascular endothelial function and exercise capacity in breast and prostate cancer survivors.

Endothelin, a peptide inhibitor of Na(+)-K(+)-ATPase in intact renaltubular epithelial cells

1989 ◽  
Vol 257 (6) ◽  
pp. C1101-C1107 ◽  
Author(s):  
M. L. Zeidel ◽  
H. R. Brady ◽  
B. C. Kone ◽  
S. R. Gullans ◽  
B. M. Brenner
Keyword(s):  
Initial Rate ◽  
Vascular Endothelial Cells ◽  
Collecting Duct ◽  
Vascular Endothelial ◽  
Na Transport ◽  
Intact Cells ◽  
Medullary Collecting Duct ◽  
Endothelin A ◽  
Potent Vasoconstrictor

Endothelin, a potent vasoconstrictor released by vascular endothelial cells, can induce natriuresis in vivo. These studies examined the regulation of Na+ transport by endothelin in suspensions of rabbit proximal tubule (PT) and inner medullary collecting duct (IMCD) cells. Endothelin reduced oxygen consumption (QO2) by 18 +/- 1% in IMCD cells but did not alter QO2 in PT cells. In IMCD cells, endothelin inhibited QO2 half maximally at approximately 5 x 10(-12) M. Several lines of evidence indicate that endothelin reduces QO2 by inhibiting the Na(+)-K(+)-ATPase. 1) Endothelin gave no further inhibition of QO2 after ouabain and blunted the stimulatory effect of amphotericin B on QO2 (+29 +/- 4% in absence of endothelin, 0 +/- 5% in presence of endothelin; n = 6 preparations, P less than 0.001). 2) Endothelin inhibited ouabain-sensitive 86Rb+ uptake by 46.6 +/- 8.6% at 10 s and by 35.4 +/- 5.3% at 30 s without altering uptake at 60 min. 3) Addition of endothelin to IMCD cells induced a net K+ efflux with an initial rate of 32.2 +/- 4.8 nmol.min-1.mg protein-1, consistent with inhibition of the Na(+)-K(+)-ATPase. In contrast to the response observed in intact cells, in permeabilized IMCD cells endothelin did not inhibit ouabain-sensitive ATPase. Several observations indicated that prostaglandin E2 (PGE2) mediates endothelin inhibition of Na(+)-K(+)-ATPase activity. 1) The response to endothelin was blocked by ibuprofen in assays of QO2, net K+ flux, and 86Rb+ uptake. 2) Endothelin and PGE2 gave equivalent, nonadditive inhibition of ouabain-sensitive 86Rb+ uptake.(ABSTRACT TRUNCATED AT 250 WORDS)

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