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

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

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

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

Endothelin(ET) is known as a family of potent hydrophobic, vasoactive peptide. We investigated the effect according to the concentrations of ET on intraocular pressure(IOP), aqueous outflow facility, pupillary diameter and light reflex and iris vessels. Twenty-four hours after injection of 2.5 microgram and 10 microgram of ET-1 into the anteriorvitreous of rabbit eyes, the IOP was reduced by 69% and 80%, respectively and did not return to the level of prefreatment until at least 14 days and 20 days, respectively. But the decrease of IOP was not due to the increased aqueous outflow. The pupillary diameter of ET-1 treated eyes was 1 to 2mm larger than the pretreatment. The time course of the pupillary effects generally ran paralled with the reduction of IOP. The iridial and conjunctival hyperemia was detectable during the pupillary dilatation. Endothelins are therefore potential participants in the local regulation of IOP, ocular blood vessel tone, and iris smooth muscle tone.
Blood Vessels ; Dilatation ; Endothelin-1* ; Endothelins ; Humans ; Hyperemia ; Intraocular Pressure ; Iris ; Muscle, Smooth ; Reflex