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*

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

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*

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

BACKGROUND: The purpose of this study was to investigate the mechanism of endothelium-dependent and independent responses to endothelins (ETs) in porcine coronary artery. METHODS: The vascular rings of left anterior descending artery or left circumflex artery from 7 pigs were suspended in conventional organ chambers for the measurement of isometric force. To evaluate relaxation responses, vascular rings with endothelium were exposed to ET-1 and ET-3. To evaluate contraction responses, vascular rings with and without endothelium were exposed to ET-1 and ET-3 in the presence or absence of BQ 123 (ET(A) receptor antagonist) or TAK-044 (ET(A) and ET(B) receptor antagonist). RESULTS: Transient relaxation responses of vascular rings occurred after exposure of ET-1 and ET-3. These transient responses disappeared after preincubation with N-nitro-L arginine. There was an increased contractions of vascular rings according to increasing concentration of ET-1 and ET-3. The initial responses were enhanced in vascular rings without endothelium in ET-1 and ET-3. In vascular rings with endothelium, the contraction responses were more reduced in vascular rings with preincubation of BQ 123 than in vascular rings without BQ 123 in ET-1. In vascular rings without endothelium, the contraction responses were more reduced in vascular rings with preincubation of TAK-044 than in vascular rings without TAK-044 in ET-1. CONCLUSION: ET(B) receptor on the endothelium might mediate the transient vasodilator responses to ET-1 and ET-3 through release of nitric oxide in porcine coronary artery. ET(A) and ET(B) receptor on vascular smooth muscle cells might mediate vasoconstrictor responses to ETs.
Arginine ; Arteries ; Coronary Vessels* ; Endothelins* ; Endothelium ; Muscle, Smooth, Vascular ; Nitric Oxide ; Receptors, Endothelin ; Relaxation ; Swine