Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P56851 (epididymal)
 11,273 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pressor effects of porcine (ET-1) and rat (ET-3) endothelins were studied in the pithed rat along with the actions of cyclo-oxygenase inhibitors upon these responses. Indomethacin (15 mumol/kg i.v.) when given prior to endothelin had no effect on the pressor responses to ET-1 or ET-3. However, when indomethacin or piroxicam was administered between two doses of ET-1 or ET-3, the second response was significantly potentiated. This potentiation was abolished when the adrenal glands were excluded from the circulation but partially restored when neuropeptide Y (NPY) (1 nmol/kg i.v.) was administered. Radiolabeled microspheres were used to measure regional blood flow and from these measurements, regional vascular resistance was calculated. From these data, it is evident that ET-1 caused a generalized increase in vascular resistance, and only in the large intestine and epididymal fat pad was this attenuated by indomethacin. In the gastric vasculature, the effects of ET-1 were potentiated by indomethacin. In the bronchial vasculature, ET-1 caused a reduction in vascular resistance possibly due to the bronchoconstrictor actions of ET-1 and the concomitant release of vasodilators such as histamine. When the fraction of the cardiac output received by each vascular bed is taken into account, the gastrointestinal tract, kidneys, and skeletal muscle account for most of the increase in total peripheral resistance induced by ET-1. Prostanoids have a role in the pressor response to ET-1 and ET-3 that is more complex than one of simple physiological antagonism or potentiation at the level of the vascular smooth muscle and possibly act as modulators of other regulatory factors such as NPY.
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PMID:The hemodynamic effects of endothelin-1 in the pithed rat. 247 37

Endothelins (ETs) are a family of vasoconstrictor and mitogenic peptides originally isolated from the endothelial cells. Three isoforms of ET, namely ET-1, ET-2 and ET-3, are generated from their respective intermediate precursors big ETs through specific endoproteolytic cleavage by endothelin converting enzyme (ECE). Using reverse-transcription polymerase chain reaction (RT-PCR), we have isolated a cDNA encoding for ECE from both the prostatic and epididymal halves of rat vas deferens. In situ hybridization using digoxigenin-labeled ECE cDNA probe demonstrated that ECE mRNA is preferentially localized in the inner longitudinal smooth muscle layer adjacent to submucosa region of rat vas deferens. Both ET-1 and big ET-1 at 30 nM potentiated electrically stimulated contractile response of prostatic vas deferens. Pre-incubation of tissue with a metalloprotease ECE inhibitor phosphoramidon (10 microM) strongly inhibited the response to big ET-1, but not to ET-1. On the other hand, big ET-1 failed to elicit contractile response of epididymal vas deferens. Phosphoramidon alone did not affect both the basal and electrically stimulated contractile responses in vas deferens. These data indicate that the circulating ET-1 and its immediate precursor big ET-1 could differentially regulate smooth muscle contractions in the prostatic and epididymal vas deferens of the rat.
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PMID:Expression and localization of endothelin converting enzyme in rat vas deferens. 912 83

We observed endothelin (ET)-induced contractile responses on prostatic and epididymal segments, as well as the facilitation of an electrically stimulated tone on prostatic segments of isolated rat vas deferens. In both segments, the selective ET(B)-receptor agonists, IRL 1620 and sarafotoxin S6c, produced only a small contraction or no contraction at a concentration of 1 microM. The rank order of contraction potencies (pD2 value) was ET-1 = ET-2 > ET-3 >> sarafotoxin S6c = IRL 1620. The maximum responses of ET-induced contractions in the prostatic segments were larger than those in the epididymal segments. The contractile response to ET-3 was antagonized by pretreatment for 30 min with BQ-123 (10 nM), a selective ET(A) receptor antagonist, and BQ-788 (1 microM), a selective ET(B) receptor antagonist. The contractile responses to ET-1 were antagonized by pretreatment with BQ-123 (10 microM), but not with BQ-788 (1 microM). The ET-3-induced facilitation on the twitch response to electrical stimulation in the prostatic segment of the vas deferens was antagonized by BQ-123 (0.1 microM) and BQ-788 (1 microM). The ET-1-induced facilitation was antagonized by pretreatment with BQ-123 (3 microM), but not with BQ-788 (10 microM). These results suggest that in rat vas deferens the ET(A) receptors are divided into BQ-123-sensitive ET(A1) and BQ-123-insensitive ET(A2) subtypes, and the production of a contractile response of smooth muscle as well as the facilitation of neurotransmission are accomplished through mediation by ET(A1)- and ET(A2)-subtypes.
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PMID:The characteristics of endothelin receptor subtypes on muscle contraction and neuro-transmission in rat vas deferens. 970 56

The specificity of endothelin (ET) receptors involved in the inhibition of insulin-stimulated glucose uptake (ISGU) in rat adipocytes was investigated. Adipocytes were isolated from the epididymal fat pads of Sprague-Dawley rats. To determine receptor subtypes, we used three ET isopeptides, ET-1 and ET-2, both of which are nonselective agonists, and ET-3, a selective agonist for ETC receptors, to displace [125I]ET-1 binding from the fat cells. The efficiency of displacement was ET-1 > ET-2 >> ET-3, indicating that the primary receptors involved belonged to the ETA subtype. At an equal concentration of 1 micromol/L, BQ-610, a selective ETA antagonist, displaced [125I]ET-1 from binding to fat cells, whereas IRL-1038, a selective ETB antagonist, did not. Using [3H]2-deoxy-D-1-glucose ([3H]2-DG) as a tracer in studies of glucose uptake, we found that equimolar BQ-610 completely reversed the inhibitory effect of ET-1 on ISGU, whereas IRL-1038 was ineffective. Northern blot analysis of adipocyte receptors showed abundant mRNA for ETA, but no ETB subtype. These results clearly demonstrate that ETA is the predominant receptor in rat adipocytes.
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PMID:Evidence that endothelin-1 (ET-1) inhibits insulin-stimulated glucose uptake in rat adipocytes mainly through ETA receptors. 986 75