Effects of exercise training on expression of endothelin-1 mRNA in the aorta of aged rats

2002 ◽  
Vol 103 (s2002) ◽  
pp. 118S-123S ◽  
Author(s):  
Seiji MAEDA ◽  
Takashi MIYAUCHI ◽  
Motoyuki IEMITSU ◽  
Takumi TANABE ◽  
Tomoko YOKOTA ◽  
...  
Keyword(s):  
Exercise Training ◽  
Endothelial Function ◽  
Vascular Endothelial Cells ◽  
Young Group ◽  
Aged Rats ◽  
Aged Group ◽  
Endothelin 1 ◽  
Real Time Quantitative Pcr ◽  
Vascular Tonus ◽  
Potent Vasoconstrictor

Aging impairs endothelial function and the vascular tone regulation, although the precise mechanism remains unclear. Endothelin-1 (ET-1) is a potent vasoconstrictor peptide produced by vascular endothelial cells. Because ET-1 has a potent vasoconstrictor effect on vessels, it may be involved in the regulation of vascular tonus. We hypothesized that aging causes a decrease in ET-1 expression in aorta, and that exercise training improves the aging-induced decrease in ET-1 expression in aorta. This study was performed to examine whether gene expression of ET-1 in the aorta of rats is altered by aging and subsequent exercise training. We studied expression of ET-1 mRNA in the aortas of sedentary young rats (Sedentary young group, 4 months old), sedentary aged rats (Sedentary aged group, 23 months old), and swim trained aged rats (Training aged group, 23 months old; swimming training for 8 weeks, 5days/week, 90min/day). The expression of ET-1 mRNA in the aorta was analysed by real-time quantitative PCR. Body weight and resting heart rate were significantly lower in the Training aged group compared with the Sedentary aged group. These results suggest that the Training aged rats exhibited physiological effects from exercise training. The expression of ET-1 mRNA in the aorta was markedly lower in Sedentary aged group compared with the Sedentary young group, whereas it was significantly higher in Training aged group compared with the Sedentary aged group. These results show that the expression of ET-1 mRNA in the aorta is decreased by aging, and that the expression is increased by exercise training. Therefore, the present study provides a possibility that exercise training improves endothelial function through up-regulation of the aging-induced decrease in ET-1 expression in the aorta.

Effects of aging and subsequent exercise training on gene expression of endothelin-1 in rat heart

2002 ◽  
Vol 103 (s2002) ◽  
pp. 152S-157S ◽  
Author(s):  
Motoyuki IEMITSU ◽  
Takashi MIYAUCHI ◽  
Seiji MAEDA ◽  
Takumi TANABE ◽  
Yoko IRUKAYAMA-TOMOBE ◽  
...  
Keyword(s):  
Gene Expression ◽  
Exercise Training ◽  
Cardiac Hypertrophy ◽  
Mrna Expression ◽  
Natriuretic Peptide ◽  
Young Group ◽  
Aged Rats ◽  
Aged Group ◽  
Endothelin 1 ◽  
Rat Hearts

Endothelin-1 (ET-1) is produced by endothelial cells and cardiac myocytes. ET-1 has potent positive inotropic and chronotropic effects on heart and induces myocardial cell hypertrophy. We investigated whether gene expression of ET-1 in rat hearts is altered by aging and subsequent exercise training. We also investigated whether gene expression of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), which participate in some pathological cardiac conditions, in the rat hearts is altered by aging and subsequent exercise training. We studied mRNA expression of ET-1, ANP and BNP in hearts of sedentary young rats (Sedentary young; 4 months old), sedentary aged rats (Sedentary aged; 23 months old), and swim-trained aged rats (Trained aged; 23 months old, swimming training for 8 weeks). The left ventricle weight mass index for body weight and left ventricular end-diastolic dimension were significantly higher in the Trained aged group compared with the Sedentary aged group. These results showed that Trained aged rats developed cardiac hypertrophy with improvement of cardiac function. The mRNA expression of ET-1 in the heart was significantly higher in Sedentary aged group compared with Sedentary young group, and was significantly higher in the Trained aged group compared with the Sedentary aged group. The mRNA expression of ANP and BNP in the heart was significantly higher in Sedentary aged group compared with Sedentary young group, and was significantly higher in the Trained aged group compared with the Sedentary aged group. The present results show that mRNA expression of ET-1 in the heart is increased by aging, and that the mRNA expression is further increased by exercise-induced cardiac hypertrophy, suggesting that ET-1 in the heart may participate in these physiological cardiac adaptations.

Muscle microvascular adaptation and angiogenic gene induction in response to exercise training are attenuated in middle-aged rats

2015 ◽  
Vol 11 (1) ◽  
pp. 23-33
Author(s):  
J. Suzuki
Keyword(s):  
Exercise Training ◽  
Acute Exercise ◽  
Young Group ◽  
Treadmill Running ◽  
Mrna Levels ◽  
Aged Rats ◽  
Middle Aged ◽  
Vegf Mrna ◽  
Aged Group ◽  
Exercise Induced

This study was designed to investigate exercise-induced changes in muscle capillarisation, the mRNA expression of angiogenic genes, and microRNA levels in young and middle-aged rats. Rats in the training groups were subjected to treadmill running 5 days a week for 3 weeks. The exercise protocol for the young (12-week old) group was 20-25 m/min, 40-60 min/day with a gradient of 15%, and for the middle-aged (12-month old) group was 18-20 m/min, 40-60 min/day with a gradient of 5%. The enzyme histochemical identification of capillary profiles was performed on cross-sections of gastrocnemius muscle. Total RNA was isolated, reverse transcription was performed, and mRNA and microRNA levels were determined by real-time PCR. The capillary-to-fibre ratio was significantly increased by exercise training in the young group (by 10%), but only slightly in the middle-aged (by 5%) group. Vascular endothecial growth factor (VEGF) mRNA levels were at significantly higher values after acute exercise (1.6-fold) and the 3-week training protocol (1.9-fold) in the young group, but not in the middle-aged group. VEGF protein expression levels were significantly increased after training in the young group only. Endothelial nitric oxide synthase, VEGF-R2 and thrombospondin-1 mRNA levels were significantly lower in the middle-aged group than in the young group. Anti-angiogenic miR-195 levels were significantly enhanced by exercise training in the middle-aged group only. These results indicated that the exercise-induced adaptation of muscle capillarity was attenuated in middle-aged rats, possibly by the lower induction of VEGF and up-regulation of anti-angiogenic miRNA expression.

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 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 Exercise Training Could Improve Age-Related Changes in Cerebral Blood Flow and Capillary Vascularity through the Upregulation of VEGF and eNOS

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Sheepsumon Viboolvorakul ◽  
Suthiluk Patumraj
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Exercise Training ◽  
Young Group ◽  
Aged Group ◽  
Protein Levels ◽  
Microvascular Changes ◽  
Age Related ◽  
Male Wistar Rats ◽  
Endothelial Nitric Oxide

This study aimed to investigate the effect of exercise training on age-induced microvascular alterations in the brain. Additionally, the association with the protein levels of vascular endothelial growth factor (VEGF) and endothelial nitric oxide synthase (eNOS) was also assessed. Male Wistar rats were divided into four groups: sedentary-young (SE-Young,n=5), sedentary aged (SE-Aged,n=8), immersed-aged (IM-Aged,n=5), and exercise trained-aged (ET-Aged, 60 minutes/day and 5 days/week for 8 weeks,n=8) rats. The MAPs of all aged groups, SE-Aged, IM-Aged, and ET-Aged, were significantly higher than that of the SE-Young group. The regional cerebral blood flow (rCBF) in the SE-Aged and IM-Aged was significantly decreased as compared to SE-Young groups. However, rCBF of ET-Aged group was significantly higher than that in the IM-Aged group (P<0.05). Moreover, the percentage of capillary vascularity (%CV) and the levels of VEGF and eNOS in the ET-Aged group were significantly increased compared to the IM-Aged group (P<0.05). These results imply that exercise training could improve age-induced microvascular changes and hypoperfusion closely associated with the upregulation of VEGF and eNOS.

Alteration of plasma endothelin-1 by exercise at intensities lower and higher than ventilatory threshold

1994 ◽  
Vol 77 (3) ◽  
pp. 1399-1402 ◽  
Author(s):  
S. Maeda ◽  
T. Miyauchi ◽  
K. Goto ◽  
M. Matsuda
Keyword(s):  
Plasma Concentration ◽  
Ventilatory Threshold ◽  
Vascular Endothelial Cells ◽  
Plasma Concentrations ◽  
Cycle Ergometer ◽  
Intercollegiate Athletes ◽  
Endothelin 1 ◽  
Ergometer Exercise ◽  
Before And After ◽  
Potent Vasoconstrictor

The purpose of this study was to investigate whether the release of endothelin-1 (ET-1), a potent vasoconstrictor peptide produced by vascular endothelial cells, is induced by exercise. Venous plasma concentrations of ET-1 were measured by sandwich-enzyme immunoassay before and after endurance exercise with a cycle ergometer at different intensities. Male intercollegiate athletes participated in the study and performed cycle ergometer exercise of 30 min duration at intensities of 90 or 130% of their individual ventilatory threshold (VT). The plasma concentration of ET-1 was slightly but significantly increased after exercise at 90% and markedly increased after exercise at 130% of individual VT. The increase in ET-1 was greatest 30 min after exercise at both intensities. It was first demonstrated that the plasma concentration of ET-1 was significantly increased after exercise: the greater the intensity, the greater the extent of the increase in plasma ET-1 concentration. However, the precise physiological roles of ET-1 during exercise remain to be elucidated.

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)

Protective Effects of Exercise Training Against Aged Induced the Reduction of Cardiac Angiogenic Capacity in Middle Aged Rats

2020 ◽  
Vol 04 (01) ◽  
Author(s):  
Titiporn Mekrungruangwong ◽  
Pimpetch Kasetsuwan ◽  
Sheepsumon Viboolvorakul ◽  
Suthiluk Patumraj
Keyword(s):  
Exercise Training ◽  
Protective Effects ◽  
Aged Rats ◽  
Middle Aged

scholarly journals Placenta growth factor augments endothelin-1 and endothelin-B receptor expression via hypoxia-inducible factor-1α

Blood ◽  
2008 ◽  
Vol 112 (3) ◽  
pp. 856-865 ◽  
Author(s):  
Nitin Patel ◽  
Caryn S. Gonsalves ◽  
Punam Malik ◽  
Vijay K. Kalra
Keyword(s):  
Growth Factor ◽  
Hypoxia Inducible Factor ◽  
Receptor Expression ◽  
Placenta Growth Factor ◽  
Promoter Regions ◽  
Endothelin B Receptor ◽  
Endothelin 1 ◽  
Hypoxia Inducible Factor 1Α ◽  
Endothelin B ◽  
Potent Vasoconstrictor

Abstract Pulmonary hypertension (PHT) develops in sickle cell disease (SCD) and is associated with high mortality. We previously showed that erythroid cells produce placenta growth factor (PlGF), which activates monocytes to induce proinflammatory cytochemokines, contributing to the baseline inflammation and severity in SCD. In this study, we observed that PlGF increased expression of endothelin-1 (ET-1) and endothelin-B receptor (ET-BR) from human pulmonary microvascular endothelial cells (HPMVECs) and monocytes, respectively. PlGF-mediated ET-1 and ET-BR expression occurred via activation of PI-3 kinase, reactive oxygen species and hypoxia inducible factor-1α (HIF-1α). PlGF increased binding of HIF-1α to the ET-1 and ET-BR promoters; this effect was abrogated with mutation of hypoxia response elements in the promoter regions and HIF-1α siRNA and confirmed by chromatin immunoprecipitation analysis. Furthermore, PlGF-mediated ET-1 release from HPMVECs and ET-BR expression in monocytes creates a PlGF–ET-1–ET-BR loop, leading to increased expression of MCP-1 and IL-8. Our studies show that PlGF-induced expression of the potent vasoconstrictor ET-1 and its cognate ET-BR receptor occur via activation of HIF-1α, independent of hypoxia. PlGF levels are intrinsically elevated from the increased red cell turnover in SCD and in other chronic anemia (eg, thalassemia) and may contribute to inflammation and PHT seen in these diseases.

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