Ignet

Gene Information

Gene symbol: EDN3

Gene name: endothelin 3

HGNC ID: 3178

Synonyms: ET3

Related Genes

#	Gene Symbol	Number of hits
1	CALCA	1 hits
2	ECE1	1 hits
3	EDN1	1 hits
4	EDN2	1 hits
5	EDNRA	1 hits
6	EDNRB	1 hits
7	FOS	1 hits
8	IL8	1 hits
9	INS	1 hits
10	MUC5B	1 hits
11	NFKB1	1 hits
12	NOS2A	1 hits
13	NOS3	1 hits
14	POMC	1 hits
15	PRL	1 hits
16	VEGFA	1 hits

Related Sentences

#	PMID	Sentence
1	1393277	Altered microvascular reactivity to endothelin-1, endothelin-3 and NG-nitro-L-arginine methyl ester in streptozotocin-induced diabetes mellitus.
2	1393277	1 We have determined the dermal microvascular effects of the nitric oxide (NO) synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME, 100 nmol/site), endothelin-1 (ET-1, 0.1-10 pmol/site) and ET-3 (0.1-30 pmol/site) in rats with streptozotocin (STZ)-induced diabetes mellitus.
3	1393277	The enantiomer D-NAME had no effect in either group of rats. 4 Low doses of ET-1 and ET-3 injected intradermally induced dose-dependent decreases in blood flow, measured by 133Xe clearance, which were similar in both groups of rats.
4	1393277	However, the responses to the highest doses of ET-1 (10 pmol/site) and ET-3 (10 and 30 pmol/site) were significantly reduced in the diabetic compared with the normal rats (P less than 0.05).In addition vasoconstriction to the highest doses of vasopressin (0.3 and 3 pmol/site) and vasodilatation to the neuropeptide calcitonin gene-related peptide (CGRP, 1O pmol/site) were similarly reduced in the diabetic rats (P <0.05).5.
5	1393277	These results indicate that the cutaneous microvasculature of rats with STZ-induced diabetes responds differently to intradermal ET-1 and ET-3 compared with normal rats; a similarly altered vascular reactivity was observed with vasopressin and CGRP.
6	1393277	Altered microvascular reactivity to endothelin-1, endothelin-3 and NG-nitro-L-arginine methyl ester in streptozotocin-induced diabetes mellitus.
7	1393277	1 We have determined the dermal microvascular effects of the nitric oxide (NO) synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME, 100 nmol/site), endothelin-1 (ET-1, 0.1-10 pmol/site) and ET-3 (0.1-30 pmol/site) in rats with streptozotocin (STZ)-induced diabetes mellitus.
8	1393277	The enantiomer D-NAME had no effect in either group of rats. 4 Low doses of ET-1 and ET-3 injected intradermally induced dose-dependent decreases in blood flow, measured by 133Xe clearance, which were similar in both groups of rats.
9	1393277	However, the responses to the highest doses of ET-1 (10 pmol/site) and ET-3 (10 and 30 pmol/site) were significantly reduced in the diabetic compared with the normal rats (P less than 0.05).In addition vasoconstriction to the highest doses of vasopressin (0.3 and 3 pmol/site) and vasodilatation to the neuropeptide calcitonin gene-related peptide (CGRP, 1O pmol/site) were similarly reduced in the diabetic rats (P <0.05).5.
10	1393277	These results indicate that the cutaneous microvasculature of rats with STZ-induced diabetes responds differently to intradermal ET-1 and ET-3 compared with normal rats; a similarly altered vascular reactivity was observed with vasopressin and CGRP.
11	1393277	Altered microvascular reactivity to endothelin-1, endothelin-3 and NG-nitro-L-arginine methyl ester in streptozotocin-induced diabetes mellitus.
12	1393277	1 We have determined the dermal microvascular effects of the nitric oxide (NO) synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME, 100 nmol/site), endothelin-1 (ET-1, 0.1-10 pmol/site) and ET-3 (0.1-30 pmol/site) in rats with streptozotocin (STZ)-induced diabetes mellitus.
13	1393277	The enantiomer D-NAME had no effect in either group of rats. 4 Low doses of ET-1 and ET-3 injected intradermally induced dose-dependent decreases in blood flow, measured by 133Xe clearance, which were similar in both groups of rats.
14	1393277	However, the responses to the highest doses of ET-1 (10 pmol/site) and ET-3 (10 and 30 pmol/site) were significantly reduced in the diabetic compared with the normal rats (P less than 0.05).In addition vasoconstriction to the highest doses of vasopressin (0.3 and 3 pmol/site) and vasodilatation to the neuropeptide calcitonin gene-related peptide (CGRP, 1O pmol/site) were similarly reduced in the diabetic rats (P <0.05).5.
15	1393277	These results indicate that the cutaneous microvasculature of rats with STZ-induced diabetes responds differently to intradermal ET-1 and ET-3 compared with normal rats; a similarly altered vascular reactivity was observed with vasopressin and CGRP.
16	1393277	Altered microvascular reactivity to endothelin-1, endothelin-3 and NG-nitro-L-arginine methyl ester in streptozotocin-induced diabetes mellitus.
17	1393277	1 We have determined the dermal microvascular effects of the nitric oxide (NO) synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME, 100 nmol/site), endothelin-1 (ET-1, 0.1-10 pmol/site) and ET-3 (0.1-30 pmol/site) in rats with streptozotocin (STZ)-induced diabetes mellitus.
18	1393277	The enantiomer D-NAME had no effect in either group of rats. 4 Low doses of ET-1 and ET-3 injected intradermally induced dose-dependent decreases in blood flow, measured by 133Xe clearance, which were similar in both groups of rats.
19	1393277	However, the responses to the highest doses of ET-1 (10 pmol/site) and ET-3 (10 and 30 pmol/site) were significantly reduced in the diabetic compared with the normal rats (P less than 0.05).In addition vasoconstriction to the highest doses of vasopressin (0.3 and 3 pmol/site) and vasodilatation to the neuropeptide calcitonin gene-related peptide (CGRP, 1O pmol/site) were similarly reduced in the diabetic rats (P <0.05).5.
20	1393277	These results indicate that the cutaneous microvasculature of rats with STZ-induced diabetes responds differently to intradermal ET-1 and ET-3 compared with normal rats; a similarly altered vascular reactivity was observed with vasopressin and CGRP.
21	1393277	Altered microvascular reactivity to endothelin-1, endothelin-3 and NG-nitro-L-arginine methyl ester in streptozotocin-induced diabetes mellitus.
22	1393277	1 We have determined the dermal microvascular effects of the nitric oxide (NO) synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME, 100 nmol/site), endothelin-1 (ET-1, 0.1-10 pmol/site) and ET-3 (0.1-30 pmol/site) in rats with streptozotocin (STZ)-induced diabetes mellitus.
23	1393277	The enantiomer D-NAME had no effect in either group of rats. 4 Low doses of ET-1 and ET-3 injected intradermally induced dose-dependent decreases in blood flow, measured by 133Xe clearance, which were similar in both groups of rats.
24	1393277	However, the responses to the highest doses of ET-1 (10 pmol/site) and ET-3 (10 and 30 pmol/site) were significantly reduced in the diabetic compared with the normal rats (P less than 0.05).In addition vasoconstriction to the highest doses of vasopressin (0.3 and 3 pmol/site) and vasodilatation to the neuropeptide calcitonin gene-related peptide (CGRP, 1O pmol/site) were similarly reduced in the diabetic rats (P <0.05).5.
25	1393277	These results indicate that the cutaneous microvasculature of rats with STZ-induced diabetes responds differently to intradermal ET-1 and ET-3 compared with normal rats; a similarly altered vascular reactivity was observed with vasopressin and CGRP.
26	1725388	Incubation of endothelin-1, endothelin-2, and endothelin-3 in urine for 5 h showed that the total amount of ir-ET decreased to less than 30% of the initial levels, suggesting that endothelins are very unstable in urine.
27	1831835	Fast protein liquid chromatographic analysis of the plasma immunoreactive endothelin of dexamethasone-treated rats showed four peaks: one in the void volume, one eluting before endothelin-3, one eluting after endothelin-3 and before endothelin-1 and one eluting in a position identical with that of endothelin-1.
28	7760309	The data show a distinct regulation of ET-1 and ET-3 in dogs.
29	8179006	Analysis of the dose-inhibition curves of both ET-1 and ET-3 for binding of each ligand indicated the presence of two classes of receptors, one class (ETA receptor) with a high affinity for ET-1 and ET-2 but a low affinity for ET-3, and the other (ETB receptor) with a high affinity for ET-1, ET-2, and ET-3.
30	8179006	ET-1 stimulated muscle contraction (50% effective concentration approximately 2 nM), whereas ET-3 did not stimulate contraction or cause relaxation.
31	8179006	One type (ETA) has a high affinity for ET-1 and ET-2 and a low affinity for ET-3, and receptor occupation results in rapid ligand internalization and muscle contraction; the other type (ETB) has a high affinity for ET-1, ET-2, and ET-3, and receptor occupation results in a lesser degree of ligand internalization than the ETA receptor and does not alter contractile behavior.
32	8179006	Analysis of the dose-inhibition curves of both ET-1 and ET-3 for binding of each ligand indicated the presence of two classes of receptors, one class (ETA receptor) with a high affinity for ET-1 and ET-2 but a low affinity for ET-3, and the other (ETB receptor) with a high affinity for ET-1, ET-2, and ET-3.
33	8179006	ET-1 stimulated muscle contraction (50% effective concentration approximately 2 nM), whereas ET-3 did not stimulate contraction or cause relaxation.
34	8179006	One type (ETA) has a high affinity for ET-1 and ET-2 and a low affinity for ET-3, and receptor occupation results in rapid ligand internalization and muscle contraction; the other type (ETB) has a high affinity for ET-1, ET-2, and ET-3, and receptor occupation results in a lesser degree of ligand internalization than the ETA receptor and does not alter contractile behavior.
35	8179006	Analysis of the dose-inhibition curves of both ET-1 and ET-3 for binding of each ligand indicated the presence of two classes of receptors, one class (ETA receptor) with a high affinity for ET-1 and ET-2 but a low affinity for ET-3, and the other (ETB receptor) with a high affinity for ET-1, ET-2, and ET-3.
36	8179006	ET-1 stimulated muscle contraction (50% effective concentration approximately 2 nM), whereas ET-3 did not stimulate contraction or cause relaxation.
37	8179006	One type (ETA) has a high affinity for ET-1 and ET-2 and a low affinity for ET-3, and receptor occupation results in rapid ligand internalization and muscle contraction; the other type (ETB) has a high affinity for ET-1, ET-2, and ET-3, and receptor occupation results in a lesser degree of ligand internalization than the ETA receptor and does not alter contractile behavior.
38	8340699	The present study was designed to assess levels of messenger RNA encoding for endothelin-1, endothelin-3, and endothelin receptors A and B in glomeruli of rats with streptozotocin-induced diabetes at 4, 12, and 24 weeks of age.
39	8340699	Insulin treatment partially ameliorated the increase in messenger RNA for endothelin-1 in the glomeruli of diabetic rats (0.3 times compared with diabetic rats without insulin treatment, p < 0.01), whereas insulin treatment did not affect messenger RNA for endothelin receptors A and B in diabetic glomeruli.
40	8340699	These findings indicate that increased endothelin-1 messenger RNA in glomeruli may be a manifestation of diabetic nephropathy, and hyperglycemia or insulin-deficiency may play a role in abnormal endothelin-1 gene regulation.
41	8470108	[Endothelin-1 and endothelin-3 in the plasma of dogs].
42	8470108	Therefore, the aim of the presented study was to develop the methodology to measure and characterize endothelin-1 (ET-1) and endothelin-3 (ET-3) in the plasma of dogs.
43	8470108	[Endothelin-1 and endothelin-3 in the plasma of dogs].
44	8470108	Therefore, the aim of the presented study was to develop the methodology to measure and characterize endothelin-1 (ET-1) and endothelin-3 (ET-3) in the plasma of dogs.
45	8937475	Receptor binding experiments with [125I]ET-1 demonstrated that the densities of ET receptors in vasa deferentia from D8, C8, D16, DI16, and C16 animals were 377 +/- 11, 255 +/- 24, 315 +/- 18, 210 +/- 12, and 214 +/- 7 fmol/mg of protein, respectively. [125I]ET-1 binding to the ET receptors was inhibited by ET-1 (non-selective), BQ 610 (ETA selective), ET-3 (ETC selective), and IRL 1620 (ETB selective) with the following rank order of Ki values: ET-1 < BQ 610 < ET-3 < < IRL 1620.
46	9279481	Endothelin-1 and endothelin-3-like immunoreactivity in the eyes of diabetic and non-diabetic BB/W rats.
47	9279481	In the present study, the distribution of immunoreactive ET-1 and ET-3 was investigated in eyes from 8 month spontaneously diabetic BB/W rats and in age matched control animals.
48	9279481	Endothelin-1 and endothelin-3-like immunoreactivity in the eyes of diabetic and non-diabetic BB/W rats.
49	9279481	In the present study, the distribution of immunoreactive ET-1 and ET-3 was investigated in eyes from 8 month spontaneously diabetic BB/W rats and in age matched control animals.
50	9357071	ET-1, ET-3, IRL 1620, and BQ 610 inhibited [125I]ET-binding to the rat ureter consistent with the predominance of ETA receptors in these tissues.
51	9357071	The subtype specificity of ET receptors in ureteral tissues was confirmed with inhibition data obtained from cloned human ETA and ETB receptors.
52	9533832	Scatchard transformation of saturation binding experiments revealed that the KD and Bmax for [125I]ET-1 and [125I]ET-3 to membranes from ciliary body were 41.7+/-9 pM and 236+/-20 fmol mg-1 protein and 37. 8+/-0.4 pM and 160+/-2.0 fmol mg-1 protein, respectively.
53	9533832	Competitive experiments in the presence of cyclic pentapeptide BQ123 (selective for ETA receptors) and BQ3020 (selective for ETB receptors), demonstrated the existence of ETA and ETB receptors in a ratio of 35:65.
54	9533832	Cross-linking of [125I]ET-1 and [125I]ET-3 to ciliary body membranes resulted in the labeling of two bands with apparent molecular masses of 52 and 34 kDa, suggesting that ETA and ETB receptors have similar molecular mass.
55	9533832	Autoradiographic results show that specific [125I]ET-1 binding sites, displaced by BQ123 and BQ3020, are localized to the ciliary epithelium, supporting the idea that ETA and ETB subtype receptors exist in this tissue.
56	9533832	Scatchard transformation of saturation binding experiments revealed that the KD and Bmax for [125I]ET-1 and [125I]ET-3 to membranes from ciliary body were 41.7+/-9 pM and 236+/-20 fmol mg-1 protein and 37. 8+/-0.4 pM and 160+/-2.0 fmol mg-1 protein, respectively.
57	9533832	Competitive experiments in the presence of cyclic pentapeptide BQ123 (selective for ETA receptors) and BQ3020 (selective for ETB receptors), demonstrated the existence of ETA and ETB receptors in a ratio of 35:65.
58	9533832	Cross-linking of [125I]ET-1 and [125I]ET-3 to ciliary body membranes resulted in the labeling of two bands with apparent molecular masses of 52 and 34 kDa, suggesting that ETA and ETB receptors have similar molecular mass.
59	9533832	Autoradiographic results show that specific [125I]ET-1 binding sites, displaced by BQ123 and BQ3020, are localized to the ciliary epithelium, supporting the idea that ETA and ETB subtype receptors exist in this tissue.
60	9543639	Augmented retinal endothelin-1, endothelin-3, endothelinA and endothelinB gene expression in chronic diabetes.
61	10853710	Endothelin-1 and endothelin-3 stimulate insulin release by isolated rat pancreatic islets.
62	10853710	In vivo infusion of ET-1 in rats induces hypoglycaemia and hyperinsulinemia and in vitro incubation with ET-1 stimulates insulin release by mouse islets.
63	10853710	Islets were incubated with increasing ET-1 or ET-3, with or without glucose 5.6 mM.
64	10853710	Incubation in medium containing ET-1 and ET-3, in the presence of glucose and calcium, induced an increase in insulin release.
65	10853710	When ET-1 and ET-3 were incubated without glucose and calcium, insulin release was not modified.
66	10853710	Our studies demonstrate that: 1) ET-3, like ET-1, stimulates insulin release by rat isolated islets; 2) direct insulin stimulating effect on islets of both ET-1 and ET-3 is evident with physiological glucose concentrations and is calcium mediated.
67	10853710	Endothelin-1 and endothelin-3 stimulate insulin release by isolated rat pancreatic islets.
68	10853710	In vivo infusion of ET-1 in rats induces hypoglycaemia and hyperinsulinemia and in vitro incubation with ET-1 stimulates insulin release by mouse islets.
69	10853710	Islets were incubated with increasing ET-1 or ET-3, with or without glucose 5.6 mM.
70	10853710	Incubation in medium containing ET-1 and ET-3, in the presence of glucose and calcium, induced an increase in insulin release.
71	10853710	When ET-1 and ET-3 were incubated without glucose and calcium, insulin release was not modified.
72	10853710	Our studies demonstrate that: 1) ET-3, like ET-1, stimulates insulin release by rat isolated islets; 2) direct insulin stimulating effect on islets of both ET-1 and ET-3 is evident with physiological glucose concentrations and is calcium mediated.
73	10853710	Endothelin-1 and endothelin-3 stimulate insulin release by isolated rat pancreatic islets.
74	10853710	In vivo infusion of ET-1 in rats induces hypoglycaemia and hyperinsulinemia and in vitro incubation with ET-1 stimulates insulin release by mouse islets.
75	10853710	Islets were incubated with increasing ET-1 or ET-3, with or without glucose 5.6 mM.
76	10853710	Incubation in medium containing ET-1 and ET-3, in the presence of glucose and calcium, induced an increase in insulin release.
77	10853710	When ET-1 and ET-3 were incubated without glucose and calcium, insulin release was not modified.
78	10853710	Our studies demonstrate that: 1) ET-3, like ET-1, stimulates insulin release by rat isolated islets; 2) direct insulin stimulating effect on islets of both ET-1 and ET-3 is evident with physiological glucose concentrations and is calcium mediated.
79	10853710	Endothelin-1 and endothelin-3 stimulate insulin release by isolated rat pancreatic islets.
80	10853710	In vivo infusion of ET-1 in rats induces hypoglycaemia and hyperinsulinemia and in vitro incubation with ET-1 stimulates insulin release by mouse islets.
81	10853710	Islets were incubated with increasing ET-1 or ET-3, with or without glucose 5.6 mM.
82	10853710	Incubation in medium containing ET-1 and ET-3, in the presence of glucose and calcium, induced an increase in insulin release.
83	10853710	When ET-1 and ET-3 were incubated without glucose and calcium, insulin release was not modified.
84	10853710	Our studies demonstrate that: 1) ET-3, like ET-1, stimulates insulin release by rat isolated islets; 2) direct insulin stimulating effect on islets of both ET-1 and ET-3 is evident with physiological glucose concentrations and is calcium mediated.
85	10853710	Endothelin-1 and endothelin-3 stimulate insulin release by isolated rat pancreatic islets.
86	10853710	In vivo infusion of ET-1 in rats induces hypoglycaemia and hyperinsulinemia and in vitro incubation with ET-1 stimulates insulin release by mouse islets.
87	10853710	Islets were incubated with increasing ET-1 or ET-3, with or without glucose 5.6 mM.
88	10853710	Incubation in medium containing ET-1 and ET-3, in the presence of glucose and calcium, induced an increase in insulin release.
89	10853710	When ET-1 and ET-3 were incubated without glucose and calcium, insulin release was not modified.
90	10853710	Our studies demonstrate that: 1) ET-3, like ET-1, stimulates insulin release by rat isolated islets; 2) direct insulin stimulating effect on islets of both ET-1 and ET-3 is evident with physiological glucose concentrations and is calcium mediated.
91	10871206	We have previously shown that mRNA levels for ET-1, ET-3, and their receptors are upregulated under hyperhexosemic conditions.
92	10871206	Semiquantitative reverse transcription-polymerase chain reaction for fibronectin and collagen alpha1 (IV) was conducted after 1 month of follow-up with comparison to beta-actin housekeeping gene using slot blot hybridization and densitometry.
93	10950122	Increased transendothelial permeability was noted in cells cultured in high glucose or when the cells grown in low (physiologic) glucose were incubated with ET-1, vascular endothelial growth factor (VEGF), or N (G) -nitro-L-arginine methyl ester but not when they were incubated with ET-3, N(G)-nitro-D-arginine methyl ester, or L-glucose.
94	10950122	ET-1 immunoreactivity was blocked by the protein kinase C (PKC) inhibitor chelerythrine, the specific PKC isoform inhibitor 379196, VEGF-neutralizing antibody, or the ET(A) blocker TBC11251, but was not blocked by the specific ET(B) blocker BQ788 or by a VEGF-non-neutralizing antibody.
95	10950122	ET-1 expression and increased permeability may occur secondary to PKC isoform activation and may be modulated by VEGF and nitric oxide.
96	10989958	The investigation was conducted to study the effects of endothelin-1 (ET-1) and endothelin-3 (ET-3) on adrenocorticotropin (ACTH), cortisol and prolactin release in man.
97	10989958	After infusion of either 20 ng/min x kg ET-1, ET-3 or normal saline, venous blood samples were drawn 12 times for determination of ACTH, cortisol and prolactin during the pre- within- and postinfusion period.
98	10989958	ET-1 infusion induced a significant increase of plasma ACTH (p< 0.009) and prolactin (p<0.0001) whereas cortisol levels increased without reaching significance (p<0.074).
99	10989958	Infusion of ET-3 induced no changes in plasma levels of ACTH, cortisol or prolactin.
100	10989958	The parallel increase of ACTH and prolactin induced by infusion of ET-1 could indicate an involvement of corticotropin-releasing hormone (CRH) in mediating the ET-1 effect on the HPA-axis in man.
101	10989958	The investigation was conducted to study the effects of endothelin-1 (ET-1) and endothelin-3 (ET-3) on adrenocorticotropin (ACTH), cortisol and prolactin release in man.
102	10989958	After infusion of either 20 ng/min x kg ET-1, ET-3 or normal saline, venous blood samples were drawn 12 times for determination of ACTH, cortisol and prolactin during the pre- within- and postinfusion period.
103	10989958	ET-1 infusion induced a significant increase of plasma ACTH (p< 0.009) and prolactin (p<0.0001) whereas cortisol levels increased without reaching significance (p<0.074).
104	10989958	Infusion of ET-3 induced no changes in plasma levels of ACTH, cortisol or prolactin.
105	10989958	The parallel increase of ACTH and prolactin induced by infusion of ET-1 could indicate an involvement of corticotropin-releasing hormone (CRH) in mediating the ET-1 effect on the HPA-axis in man.
106	10989958	The investigation was conducted to study the effects of endothelin-1 (ET-1) and endothelin-3 (ET-3) on adrenocorticotropin (ACTH), cortisol and prolactin release in man.
107	10989958	After infusion of either 20 ng/min x kg ET-1, ET-3 or normal saline, venous blood samples were drawn 12 times for determination of ACTH, cortisol and prolactin during the pre- within- and postinfusion period.
108	10989958	ET-1 infusion induced a significant increase of plasma ACTH (p< 0.009) and prolactin (p<0.0001) whereas cortisol levels increased without reaching significance (p<0.074).
109	10989958	Infusion of ET-3 induced no changes in plasma levels of ACTH, cortisol or prolactin.
110	10989958	The parallel increase of ACTH and prolactin induced by infusion of ET-1 could indicate an involvement of corticotropin-releasing hormone (CRH) in mediating the ET-1 effect on the HPA-axis in man.
111	11139780	Endothelins (ETs) mediate paracrine control of vascular tone and secretion of steroids and catecholamines in the adrenal gland through two ET receptor subtypes, ETA and ETB.
112	11139780	The densities, pharmacological properties and distribution of ET receptor subtypes ETA and ETB in adrenal glands from streptozotocin-induced diabetic, insulin-treated diabetic and age-matched control rats were investigated, using radioligand receptor binding and autoradiographic techniques.
113	11139780	The gene expression of ETA and ETB receptors ET-1, ET-3 and ECE-1 was evaluated using relative multiplex reverse transcription/PCR.
114	11139780	The expression level of ET-1 mRNA was up-regulated, whereas ET-3 mRNA was down-regulated in the diabetic adrenal gland compared with the controls.
115	11139780	Autoradiographic studies showed that ETA and ETB are the predominant receptor subtypes in the adrenal medulla and cortex respectively.
116	11139780	These results suggest that ETA and ETB receptors are differentially distributed and regulated in the diabetic rat adrenal gland.
117	11139780	Endothelins (ETs) mediate paracrine control of vascular tone and secretion of steroids and catecholamines in the adrenal gland through two ET receptor subtypes, ETA and ETB.
118	11139780	The densities, pharmacological properties and distribution of ET receptor subtypes ETA and ETB in adrenal glands from streptozotocin-induced diabetic, insulin-treated diabetic and age-matched control rats were investigated, using radioligand receptor binding and autoradiographic techniques.
119	11139780	The gene expression of ETA and ETB receptors ET-1, ET-3 and ECE-1 was evaluated using relative multiplex reverse transcription/PCR.
120	11139780	The expression level of ET-1 mRNA was up-regulated, whereas ET-3 mRNA was down-regulated in the diabetic adrenal gland compared with the controls.
121	11139780	Autoradiographic studies showed that ETA and ETB are the predominant receptor subtypes in the adrenal medulla and cortex respectively.
122	11139780	These results suggest that ETA and ETB receptors are differentially distributed and regulated in the diabetic rat adrenal gland.
123	11444423	It is now known that there are three endothelin genes in the human genome (ET-1, ET-2, and ET-3).
124	11444423	ET-1 and ET-2 are both strong vasoconstrictors, whereas ET-3 is a potentially weaker vasoconstrictor than the other two isoforms.
125	11444423	This article summarizes the reported literature of the role of ET-1 in the development of diabetic complications, with particular focus on the possible role of ET-1 in mediating the effects of angiotensin-converting enzyme inhibitors.
126	11444423	It is now known that there are three endothelin genes in the human genome (ET-1, ET-2, and ET-3).
127	11444423	ET-1 and ET-2 are both strong vasoconstrictors, whereas ET-3 is a potentially weaker vasoconstrictor than the other two isoforms.
128	11444423	This article summarizes the reported literature of the role of ET-1 in the development of diabetic complications, with particular focus on the possible role of ET-1 in mediating the effects of angiotensin-converting enzyme inhibitors.
129	12122504	The expression levels of ET-1, ET-3, ET receptor subtypes and endothelin converting enzyme-1 (ECE-1) mRNAs were assessed by relative multiplex reverse transcription polymerase chain reaction (RT-PCR).
130	12122504	In addition, RT-PCR data show an upregulation in the expression of ETB receptor subtype, ET-1 and ECE-1 mRNA in both regions, and a downregulation in the expression of ETA receptor subtype mRNA in the dorsolateral region of the castrated rat prostate.
131	12193137	The effect of diabetes on endothelin, interleukin-8 and vascular endothelial growth factor-mediated angiogenesis in rats.
132	12193137	Studies were performed using the rat corneal angiogenesis model as a surrogate for collateralization to determine the effect of diabetes mellitus on endothelin (ET)-1, ET-3, vascular endothelial growth factor (VEGF) and interleukin-8 (IL-8)-mediated angiogenesis.
133	12193137	Studies of VEGF and IL-8 in fluid-resuscitated rats demonstrated that VEGF-mediated angiogenesis was only inhibited from 49% to 45%, but there was inhibition of IL-8-mediated angiogenesis from 62% to 31%.
134	12193137	Diabetes also appeared to inhibit IL-8-mediated angiogenesis, but had very little or no effect on ET-3- or VEGF-mediated angiogenesis.
135	12388107	High glucose-induced, endothelin-dependent fibronectin synthesis is mediated via NF-kappa B and AP-1.
136	12388107	We also examined the roles played by protein kinase C (PKC) and the transcription factors nuclear factor kappaB (NF-kappaB) and activating protein (AP)-1 with respect to such changes.
137	12388107	HG, PKC activators, and ETs (ET-1 and ET-3) that increased FN expression also caused activation of NF-kappaB and AP-1.
138	12388107	Inhibitors of both NF-kappaB and AP-1 prevented HG- and ET-induced FN production.
139	12388107	The results of this study indicate that glucose-induced increased FN production in diabetes may be mediated via ET-dependent NF-kappaB and AP-1 activation.
140	12824290	Diabetes-induced overexpression of endothelin-1 and endothelin receptors in the rat renal cortex is mediated via poly(ADP-ribose) polymerase activation.
141	12824290	We evaluated whether PARP activation is present and whether two unrelated PARP inhibitors, 3-aminobenzamide (ABA) and 1,5-isoquinolinediol (ISO), counteract overexpression of endothelin-1 (ET-1) and ET receptors in the renal cortex in short-term diabetes.
142	12824290	ET-1, ET(A), and ET(B) mRNA (ribonuclease protection assay), but not ET-3 mRNA (RT/PCR), abundance was increased in diabetic rats, and three variables were, at least, partially corrected by ISO.
143	15320471	It is now known that there are three endothelin genes in the human genome (ET-1, ET-2, and ET-3 genes).
144	15320471	ET-1 and ET-2 are both strong vasoconstrictors, whereas ET-3 is a potentially weaker vasoconstrictor compared to the other two isoforms.
145	15320471	On the contrary, Chakrabarti et al. demonstrate that retinas from the chronic diabetic BB/W rats (6 months) show an increase in ET-1, ET-3, ET(A) receptor and ET(B) receptor mRNA expressions when compared to those from control rats.
146	15320471	It is now known that there are three endothelin genes in the human genome (ET-1, ET-2, and ET-3 genes).
147	15320471	ET-1 and ET-2 are both strong vasoconstrictors, whereas ET-3 is a potentially weaker vasoconstrictor compared to the other two isoforms.
148	15320471	On the contrary, Chakrabarti et al. demonstrate that retinas from the chronic diabetic BB/W rats (6 months) show an increase in ET-1, ET-3, ET(A) receptor and ET(B) receptor mRNA expressions when compared to those from control rats.
149	15320471	It is now known that there are three endothelin genes in the human genome (ET-1, ET-2, and ET-3 genes).
150	15320471	ET-1 and ET-2 are both strong vasoconstrictors, whereas ET-3 is a potentially weaker vasoconstrictor compared to the other two isoforms.
151	15320471	On the contrary, Chakrabarti et al. demonstrate that retinas from the chronic diabetic BB/W rats (6 months) show an increase in ET-1, ET-3, ET(A) receptor and ET(B) receptor mRNA expressions when compared to those from control rats.
152	15331199	The present study investigated vascular endothelial growth factor (VEGF) and its interactions with endothelin (ET) 1 and 3, endothelial, and inducible nitric oxide synthase (eNOS, iNOS) in mediating diabetes induced retinal vascular dysfunction.
153	15331199	Male Sprague Dawley rats with streptozotocin (STZ) induced diabetes, with or without VEGF receptor signal inhibitor SU5416 treatment (high or low dose) were investigated after 4 weeks of follow-up.
154	15331199	Diabetic animals showed higher resistivity index (RI), indicative of vasoconstriction with increased ET-1 and ET-3 mRNA expression, whereas eNOS and iNOS mRNA expressions were un-affected.
155	15331199	SU5416 treatment corrected increased RI via increased iNOS in spite of increased ET-1, ET-3 and VEGF mRNA expression.
156	15331199	Cell culture (HUVEC) studies indicate that in part, an SU5416 induced iNOS upregulation may be mediated though a MAP kinase signalling pathway.
157	15331199	The present study investigated vascular endothelial growth factor (VEGF) and its interactions with endothelin (ET) 1 and 3, endothelial, and inducible nitric oxide synthase (eNOS, iNOS) in mediating diabetes induced retinal vascular dysfunction.
158	15331199	Male Sprague Dawley rats with streptozotocin (STZ) induced diabetes, with or without VEGF receptor signal inhibitor SU5416 treatment (high or low dose) were investigated after 4 weeks of follow-up.
159	15331199	Diabetic animals showed higher resistivity index (RI), indicative of vasoconstriction with increased ET-1 and ET-3 mRNA expression, whereas eNOS and iNOS mRNA expressions were un-affected.
160	15331199	SU5416 treatment corrected increased RI via increased iNOS in spite of increased ET-1, ET-3 and VEGF mRNA expression.
161	15331199	Cell culture (HUVEC) studies indicate that in part, an SU5416 induced iNOS upregulation may be mediated though a MAP kinase signalling pathway.
162	16080914	Role of protein kinase C on the alteration of retinal endothelin-1 in streptozotocin-induced diabetic rats.
163	16080914	Retinal tissues were analysed for the expression of endothelin-1 (ET-1), endothelin-3 (ET-3), endothelin-A (ET-A), and endothelin-B (ET-B) mRNA by means of semi-quantitative RT-PCR.
164	16080914	The retina from the diabetic rats showed increased ET-1 mRNA expression after 2 weeks, while no changes were found for ET-3, ET-A and ET-B.
165	16080914	Role of protein kinase C on the alteration of retinal endothelin-1 in streptozotocin-induced diabetic rats.
166	16080914	Retinal tissues were analysed for the expression of endothelin-1 (ET-1), endothelin-3 (ET-3), endothelin-A (ET-A), and endothelin-B (ET-B) mRNA by means of semi-quantitative RT-PCR.
167	16080914	The retina from the diabetic rats showed increased ET-1 mRNA expression after 2 weeks, while no changes were found for ET-3, ET-A and ET-B.
168	21461356	Endothelin is a potent vasoactive peptide occurring in three isotypes, ET-1, ET-2, and ET-3.