No abstract available.
Endothelin-1* ; Endothelins*

No abstract available.
Endothelin-1* ; Endothelins*

Using Mercox CL-2B, intravascular casting was performed follwoing intracameral injection with 2.0microgram/microliter of Endothelin-1(ET-1) in the rabbit eye. One hour after intracameral injection with ET-1 caused severe focal andsegmental constriction of major arterial circle(MAC). Obstruction of the small branch of MAC caused localized filling defect and decreased number of capillaries in the vascular cast. The diameters of vascular cast were reduced at about 22.2% in proximal MAC, 22.4% in distal MAC and 21.8% in first branch of MAC. This results were suggested that ET-1 may play a role in the regulation of blood flow in the anterior segment vasculature of the rabbit.
Capillaries ; Constriction ; Endothelin-1* ; Microvessels*

Epidermal keratinocytes are important sources of a wide variety of cytokines that include the endothelin-1 (ET-1). Glucocorticoids have been shown to inhibit the production of several cytokines. However, their effect on ET-1 synthesis by keratinocytes is still unknown. It has been reported that ultraviolet B (UVB) irradiation stimulates both the synthesis and release of ET-1 and it was observed that ET-1 secretion by HaCat cells increased with increasing UVB exposure. In this study, the effects of glucocorticoid on ET-1 production were evaluated using cultured HaCat keratinocytes. The results showed that dexamethasone suppressed basal re-lease of ET-1. In addition, it strongly inhibited the UVB-mediated augmentation of ET-1 production. Furthermore, lincomycin slightly enhanced the inhibitory effect of dexamethasone on ET-1 synthesis.
Cytokines ; Dexamethasone* ; Endothelin-1 ; Glucocorticoids ; Keratinocytes* ; Lincomycin

In the freshly isolated rat nephron, the effect of endothelin-1, -2 and -3 (ET-1, -2 and -3) on cytosolic free calcium concentration ((Ca2+)i) was determined using the fluorescent indicator Fura-2/AM. (Ca2+)i increase was investigated in 9 parts of the single nephron including glomerulus (Glm), S1, S2, S3, Cortical and medullary thick ascending limb and cortical (CCT) and outer medullary collecting tubule (OMCT). Endothelins increased (Ca2+)i in Glm (ET-1; 127+/-17%, ET-2; 93+/-5%, ET-3; 169+/-17%), CCT (ET-1; 30+/-6%, ET-2; 38+/- 19%, ET-3; 158+/-18%) and OMCT (ET-1; 197+/- 11%, ET-2; 195+/- 11%, ET-3; 215+ 37%) at 10(-7) M. In OMCT, ET-1 and ET-2 increased (Ca2+)i in a dose-dependent manner (10(-10) ~ 10(-6) M). To the contrary, ET-3-induced (Ca2+)i rise was begun from 10(-12) M. BQ-123Na, an antagonist of ETA receptor, at 10(-4) M inhibited about 30% of (Ca2+)i rise induced by ET-1 and -3. Binding experiments using (125I)ET-3 showed the existence of ETB receptor in OMCT. This binding was replaced by ET-1, ET-2 or ET-3 by the almost same degree but not by angiotensin II or vasopressin.
Angiotensin II ; Animals ; Calcium* ; Cytosol ; Endothelin-1 ; Endothelin-2 ; Endothelins* ; Extremities ; Nephrons* ; Rats* ; Vasopressins

PURPOSE: Many kinds of substances are produced on vascular endothelial activation. The aim of this study is to confirm an increase in Endothelin-1 (ET-1), the most potent vasoconstrictor, which is produced by endothelial activation, in patients with chronic anal fissure and to infer the relationship between ET-1 and anal fissure chronicity. METHODS: The study groups are divided into three different groups with 30 subjects each. Group 1 is comprised of healthy volunteers, group 2 of chronic anal fissure patients, and Group 3 of patients with higher than 3rd degree hemorrhoids. Blood samples were taken to measure the ET-1 levels in subject's serum and to compare the results with those for the control groups. RESULTS: Among the 90 subjects, 38 were male, and 52 were female. The average age was 36.8. The average ET-1 level marked 1.47 +/- 0.78 pg/mL for male subjects and 1.16 +/- 0.47 pg/mL for female subjects (P = 0.02). The average ET-1 level in the patient groups is as follow: 1.21 +/- 0.44 pg/mL in group 1, 1.46 +/- 0.83 pg/mL in group 2, and 1.20 +/- 0.56 pg/mL in group 3 (P = 0.14). CONCLUSION: Group 2, the chronic anal fissure patient group, showed a higher ET-1 level than groups 1 and 3, the control group and the hemorrhoid patient group, but this difference had no statistical significance.
Endothelin-1 ; Endothelium ; Female ; Fissure in Ano ; Hemorrhoids ; Humans ; Ischemia ; Male

BACKGROUND: Monocyte chemoattractant protein- 1 (MCP-1) is an important mediator for monocyte/ macrophage infiltration in various inflammatory renal diseases and is produced by renal cells. In the process of renal diseases, endothelin-1 (ET-1) is known to play an active role in cell growth, inflammation and fibrosis. The aim of this study was to investigate whether three isoforms of endothelin regulate MCP-1 expression in cultured mesangial cells. METHODS: Mesangial cells were incubated with or without various doses of ET-1, ET-2 or ET-3. To determine the monocyte chemotactic activity, chemotaxis assay was performed in modified Boyden chambers using freshly isolated human monocytes. MCP-1 mRNA expression in mesangial cells was measured by Northern blot analysis. RESULTS: ET-1, ET-2 and ET-3 stimulated monocyte chemotactic activity released from mesangial cells in a dose-dependent manner. ET-1, ET-2 and ET-3 also stimulated MCP-1 mRNA expression in a time-dependent manner, which was seen as early as 4 hours and was maintained up to 24 hours. CONCLUSION: These data suggest that ET-1, ET- 2 and ET-3 stimulate MCP-1 expression in mesangial cells and may contribute to the monocyte/ macrophage infiltration in inflammatory renal diseases.
Animals ; Blotting, Northern ; Chemokine CCL2* ; Chemotaxis ; Endothelin-1* ; Endothelin-2* ; Endothelin-3* ; Endothelins ; Fibrosis ; Humans ; Inflammation ; Macrophages ; Mesangial Cells* ; Monocytes* ; Protein Isoforms ; Rats* ; RNA, Messenger

AIMTo investigate the effect of endogenous endothelin-1 (ET-1) on cardiomyocyte apoptosis induced by hypoxia and its possible mechanism.

METHODSCultured neonatal rat cardiomyocytes were divided into control group and ET receptor antagonist group. Control group was given DMEM only and ET receptor antagonist group was treated with ET receptor subtype A (ET(A)) receptor antagonist BQ610 and BQ123 or ET(B) receptor antagonist BQ788 and subjected to hypoxia for 24 h. The presence of apoptosis in cardiomyocytes was evaluated by TUNEL analysis and flow cytometry (FCM).

RESULTSTUNEL analysis showed that the percentage of positive apoptotic cells in BQ610 5 micromol/L group was 13.2% +/- 3.7%, significantly lower than that in hypoxia group (24.2% +/- 2.2%, P < 0.01). FCM showed that BQ123 (0.04, 0.2 and 1.0 micromol/L) inhibited hypoxia-induced cardiomyocyte apoptosis and increased cardiomyocyte survival rate in a dose-dependent manner, while BQ788 did not show such effects.

CONCLUSIONThese findings suggest that endogenous ET-1 aggravates hypoxia-induced cardiomyocyte apoptosis and this effect is mediated through ET(A) receptor-dependent pathways.

Animals ; Animals, Newborn ; Apoptosis ; Cell Hypoxia ; Cells, Cultured ; Endothelin A Receptor Antagonists ; Endothelin B Receptor Antagonists ; Endothelin-1 ; physiology ; Myocytes, Cardiac ; metabolism ; pathology ; Rats ; Rats, Sprague-Dawley

The correlation between pulmonary endothelin receptors and alveolar-arterial oxygen gradient (A-aDO2) in rats with hepatopulmonary syndrome was investigated. Animals were divided into 2 groups: Sham-operated (Sham) group and common bile duct ligation (CBDL) group. Arterial blood gas was evaluated by a blood gas analyzer. The concentrations of ET-1 in blood and lung tissue sample were evaluated by radioimmunoassay. The distribution and expression of two kinds of subtype receptor of ET-1, ETRA and ETRB were examined by in situ hybridization. The results showed that the level of A-aDO2 was higher in CBDL group than that in Sham group (P < 0.05). The levels of plasma and pulmonary ET-1 in CBDL group were both higher than in Sham group (P < 0.05). There was no significant difference in average A of ETRA between two groups by imaging analysis (0.21 +/- 0.06 vs 0.22 +/- 0.08, P > 0.05), while that of ETRB was higher in CBDL group than in Sham group (0.58 +/- 0.16 vs 0.28 +/- 0.07, P < 0.05). The expression of ETRB in lung was positively correlated with A-aDO2 (P < 0.05). It was concluded that the widened A-aDO2 may be related with enhancement of the expression of ETRB in lung.
Endothelin-1/metabolism ; Hepatopulmonary Syndrome/*metabolism ; Lung/*metabolism ; Oxygen/*metabolism ; Pulmonary Alveoli/*metabolism ; Rats, Wistar ; Receptor, Endothelin A/metabolism ; Receptor, Endothelin B/*metabolism

AIMThe purpose of the present study is to discuss the influence of different exercise load on the concentration of ET in plasma and myocardial cells, and the activity of ETR on myocardial cell's membrane in rats.

METHODS45 male SD rats were divided into the following 5 groups randomly: Group A (control group); Group B (45 min swim group); Group C (90 min swim group); Group D (150 min swim group); Group E (acute exhaust group). After having been trained for 8 weeks, the levels of ET and activity of ETR were measured by RIA.

RESULTSThe concentrations of ET in plasma and myocardial cells of 90 min swim group were decreased significantly (P < 0.01)and 90 min swim could reduce the activity of ETR (P < 0.01). The activity of ETR was elevated significantly in 150 min swim group (P < 0.01).

CONCLUSIONModerate exercise loads can significantly ameliorate the cardiovascular function, and high exercise loads is harmful to myocardial cells.

Animals ; Endothelin-1 ; metabolism ; Male ; Myocytes, Cardiac ; metabolism ; Physical Conditioning, Animal ; physiology ; Rats ; Rats, Sprague-Dawley ; Receptor, Endothelin A ; metabolism ; Swimming