No abstract available.
Endothelins* ; Receptors, Endothelin*

No abstract available.
Endothelin-1* ; Endothelins*

No abstract available.
Endothelin-1* ; Endothelins*

No abstract available.
Endothelins ; Endothelium ; Hypertension ; Reactive Oxygen Species

To investigate the effect of endothelin on intracellular free calcium ([Ca(2+)]i) mobilization and the existence of the endothelin receptor in cultured bovine corneal endothelial cells(BCEC), endothelin-1(ET-1) -induced [Ca(2+)]i increase was measuredby using calcium sensitive indicator, fura-2/AM, and the studies on its desensitizaton and receptor antagonists were also performed. ET-1 increased [Ca(2+)]i in a concentration-dependent manner(10(-9)M-10(-5)M) and ET-1 -unduced [Ca(2+)]i transient increase was significantly ingibited (~50%) by the pretreatment with EGTA for 1 min. Similarly, neomycin also attenuated ET-1 -unduced [Ca(2+)]i transient increase in a concentration-dependent mannet. Desensitizatin study with successive treatment of ET-1 and ET-3, and the experiments of antagonists(BQ-610 for the ET(A) receptor and BQ-788 for the ET(B) receptor) showed the presence of ET(B) receptor in BCEC. In addition, ET-1(10(-6)M) accumulated inositol trisphosphate about two folds (310+/-6.8 cpm) comparing to control(154+/-11.6 cpm) and this accumulation was significantly inhibited by the treatment with neomycin (187+/-28 cpm). These results suggest that endothelin-induced calcium mobilization is receptor-mediated response and TE(B) receptor exists in BCEC.
Calcium* ; Egtazic Acid ; Endothelins ; Endothelium, Corneal* ; Inositol ; Neomycin ; Receptors, Endothelin

OBJECTIVE: Both bronchial asthma and chronic obstructive pulmonary disease(COPD) are defined as disease entities causing sudden exacerbation of dyspnea; the former is a reversible airflow obstruction and the latter partially reversible and characterized by slowly progressive airflow obstruction. There were several reports suggesting endothelin release during an acute exacerbation of asthma and COPD, however few report showed comparative data of asthma and COPD concomitantly. The author examined the release of endothelin in COPD in comparison with those in asthmatics and healthy controls. METHODS: Plasma and 24 hour urine were collected from 33 asthmatics and 13 COPDs during an acute respiratory exacerbation and from 10 healthy controls. Endothelin was determined by radioimmmunoassay. RESULTS: Plasma endothelins were elevated in asthma and COPD and there were no significant changes compared with controls. Endothelin excretion in 24 hour urine was significantly higher in asthma and COPD than in controls. Endothelin concentrations in 24 hour urine showed a negative correlation with FEV1. CONCLUSION: Endothelins in 24 hour urine were increased in acute exacerbation of asthma and COPD and these increases were negatively correlated with FEV1 significantly. These findings are interpreted that endothelin contributes to the pathogenesis of acute exacerbation in asthma and COPD.
Asthma* ; Dyspnea ; Endothelins* ; Plasma ; Pulmonary Disease, Chronic Obstructive*

BACKGROUND: Recent studies have documented increased release of endothelin(ET) during acute attack of asthma. The purpose of this study is to observe the link between plasma level and urinary excretion of each and changes during acute exacerbation. METHOD: Plasma and 24 hour urine were collected from sixteen asthmatics during acute exacerbation, twice ; first day of symptomatic exacerbation and two weeks after treatment. Controls were ten healthy normal subjects. All patients were treated with corticosteroid and beta-2 adrenergic agonist on admission. ET was determined by radioimmmunoassay and had 100% cross reactivity with ET-1, 67% with ET-2, 84% with ET-3, and 8% with Big-ET. RESULTS: Plasma ETs were significantly elevated during acute attack of asthma compared with those in remission and controls. However, there was no significant changes in urine ET concentrations or total ET amounts in 24 hour urine during exacerbation upto two weeks. Those levels of urine ET in asthmatics were still higher than controls. ET concentrations in plasma or urine were not correlated with pulmonary functional parameters and hypoxemia. CONCLUSION: The findings suggests that increased plasma ETs are related with exaggerated release during acute asthma. Urinary ET excretion is increased in asthma. However, urine ET changes during exacerbation should be observed in a larger and longer scale.
Adrenergic Agonists ; Anoxia ; Asthma* ; Endothelin-2 ; Endothelins* ; Humans ; Plasma*

Animals ; Endothelins ; physiology ; Humans ; Mice ; Pulmonary Fibrosis ; etiology ; Rats

No abstract available.
Angiotensin II ; Angiotensins ; Endothelial Cells ; Endothelins ; Epoprostenol ; Thrombin ; Umbilical Veins

Glomerular mesangial cells have receptors to various growth factors and vasoactive peptides such as platelet-derived growth factor(PDGF), and endothelin(ET), which are important mediators for the progression of glomerular diseases. Heparin has been reported to have anti-proliferative effects in vascular smooth muscle cells and mesangial cells. Furthermore, the treatment with heparin suppresses the progression of experimental mesangioproliferative glomerulonephritis. The present study was carried out to further ascertain inhibitory effects of heparin and possible mechanisms of its action, particularly in relation to the effect on ET production of mesangial cells. The effect of heparin on PDGF-stimulated proliferation was assessed by [3H]thymidine uptake as well as the increase of number of cells, and ET production was evaluated in cultured rat mesangial cells. The results were as follows: 1) PDGF at a concentration of 10 ng/ml stimulated [3H]thymidine uptake significantly(mean+/-S.D., 512.0+/-38.6 cpm/well vs. 3300.4+/-432.5, p<0.05), and also increased the number of cells significantly, compared to control(23.0+/-3.5X10(3)/well vs. 66.5+/-8.9, p<0.05). 2) Heparin inhibited the PDGF(10ng/ml)-stimulated proliferation of mesangial cells in a dose-dependent manner(100microgram/ml, 3300.4+/-432.5cpm/well vs. 1452.5+/-264.7, 66.5+/-8.9 cpm/well vs. 20.0+/-6.5, p<0.05). 3) While N-desulfated heparin did not show the inhibitory effect on [3H]thymidine uptake, the potency of intact heparin(100microgram/ml) was 56.2+/-8.0% inhibition, which was similar to chondroitin sulfate(48.9+/-5.4%). N-desulfated N-acetylated heparin showed 25.7+/-9.7% inhibition. 4) PDGF stimulated the production of ET in a dose-dependent manner(25ng/ml, 4.2+/-0.7pg/ml/mg of protein vs 15.7+/-1.4, p<0.05). 5) Heparin inhibited the PDGF(25ng/ml)-stimulated ET production in a dose-dependent pattern(100microgram/ml, 12.6+/-3.5 vs. 2.5+/-1.1, p<0.05). From the above results, it is concluded that heparin has a significant inhibitory effect on proliferation and ET production in mesangial cells, and this anti-proliferative effect of heparin appears to be related to the structure of heparin, especially N-sulfation. In conclusion, heparin may reduce glomerular injury through these inhibitory effects on mesangial cells, but the further studies such as in vivo experiments considering the anticoagulation effect are needed.
Animals ; Chondroitin ; Endothelins* ; Glomerulonephritis ; Heparin* ; Intercellular Signaling Peptides and Proteins ; Mesangial Cells* ; Muscle, Smooth, Vascular ; Peptides ; Rats