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Noradrenergic Control of Arginine Vasopressin Release from the Ewe Hypothalamus In Vitro : Sensitivity to Oestradiol
Author(s) -
Ghuman SPS,
Prabhakar S,
Smith RF,
Dobson H
Publication year - 2008
Publication title -
reproduction in domestic animals
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.546
H-Index - 66
eISSN - 1439-0531
pISSN - 0936-6768
DOI - 10.1111/j.1439-0531.2007.00863.x
Subject(s) - vasopressin , endocrinology , medicine , agonist , methoxamine , hypothalamus , chemistry , antagonist , preoptic area , median eminence , arginine , receptor , biology , amino acid , biochemistry
Contents The present study aims at ascertaining the influence of α 1 ‐adrenoreceptors on arginine vasopressin (AVP) release in vitro and determine whether E 2 modulates the α 1 ‐adrenoreceptor and AVP interaction. Ten minutes after ewe killing, sagittal midline hypothalamic slices (from the anterior preoptic area to the mediobasal hypothalamus with the median eminence, 2 mm thick, 2 per sheep) were dissected, placed in oxygenated minimum essential media‐ α (MEM‐ α ) at 4°C and within 2 h were singly perifused at 37°C with oxygenated MEM‐ α (pH 7.4; flow rate 0.15 ml/min), either with or without E 2 (24 pg/ml). After 4 h equilibration, 10 min fractions were collected for 4 h interposed with 10 min exposure at 60 min to a specific α 1 ‐adrenoreceptor agonist or antagonist at various doses (0.1–10 m m ). At the end of all perifusions, slices responded to KCl (100 m m ) with AVP efflux (p < 0.05). Release of AVP was enhanced (p < 0.05) by the α 1 ‐adrenoreceptor agonist (methoxamine 10 m m ; no E 2 , n = 7 perifusion chambers: from 14.3 ± 2.7 to 20.9 ± 3.9, with E 2 , n = 10: from 10.7 ± 1.2 to 18.4 ± 3.4 pg/ml) or the antagonist (thymoxamine 10 m m ; no E 2 , n = 5: from 9.5 ± 3.1 to 30.4 ± 6.0, with E 2 , n = 10: from 10.8 ± 0.9 to 39.1 ± 6.3 pg/ml). With the agonist, the response occurred only at 80 min (p < 0.05) both in the presence and absence of E 2 . Whereas, after the antagonist, values were higher (p < 0.05) throughout the post‐treatment period (80–170 min) without E 2 , but declined by 150 min in the presence of E 2 . Furthermore, the response to the α 1 ‐adrenoreceptor antagonist was greater (p < 0.05; 90–140 min) than the agonist only in the presence of E 2 . In conclusion, these results reveal direct α 1 ‐adrenoreceptor‐mediated control of the hypothalamic AVP neuronal system which is modulated by E 2 .