Guibbolini M E, Lahlou B
Laboratoire de Physiologie Cellulaire et Comparée, Université de Nice, Parc Valrose, France.
Am J Physiol. 1990 Jan;258(1 Pt 2):R3-9. doi: 10.1152/ajpregu.1990.258.1.R3.
Arginine vasotocin (AVT) and isotocin (IT) induced direct inhibition of adenylate cyclase activity in gill plasma membranes of the rainbow trout adapted to freshwater (FW) and seawater (SW). The maximal inhibition was obtained with 10(-11)-10(-10) M (50% inhibitory concentration approximately 10(-13) M), values in agreement with the circulating levels of AVT in trout blood. Specific V1 or V2 agonists or antagonists (with reference to vasopressin) were used to define the specificity of the neurohypophysial peptide receptors involved in this inhibition. The V1 agonist [Phe2,Orn8]vasotocin ([Phe2]OVT) inhibited the basal and glucagon-stimulated adenylate cyclase activity, and this effect in SW (20%) was twice more than in FW (10%). The V2 agonist 1-deamino[Val4,Arg8]-vasopressin (dVDAVP), however, produced a stimulation that was of the same amplitude (10%) in both media. The V1 antagonist [(1-beta-mercapto-beta-beta-cyclopentamethylenepropionic acid), 1-(O-ethyl)Tyr2,Orn8]vasotocin (d(CH2)5[Tyr(Et)2]OVT) totally reversed the AVT- or IT-induced inhibition of basal or glucagon-stimulated cyclase activity, whereas the V1/V2 antagonist [(1-beta-mercapto-beta-beta-cyclopentamethylene propionic acid), 1-(O-ethyl)D-Tyr2,Val4,Arg8]vasopressin (d(CH2)5[D-Tyr(Et)2]-VAVP) (previously used as V2 antagonist in amphibians) had no such effect. When active, all analogues had their maximal activity at 10(-11)-10(-10) M (50% maximal activity approximately 10(-13) M), as observed with the natural peptides. These results, together with our previous observations, point to the gill epithelium as a direct target organ for neurohypophysial peptides and suggest that the hormone receptors involved in fish belong predominantly, if not exclusively, to a new type that we propose to designate as fish neurohypophysial hormone (NHF) receptors while awaiting further characterization.
精氨酸血管加压素(AVT)和异催产素(IT)可直接抑制适应淡水(FW)和海水(SW)环境的虹鳟鱼鳃质膜中的腺苷酸环化酶活性。在10⁻¹¹ - 10⁻¹⁰ M时可获得最大抑制效果(50%抑制浓度约为10⁻¹³ M),该数值与虹鳟鱼血液中AVT的循环水平相符。使用特异性的V1或V2激动剂或拮抗剂(参照血管加压素)来确定参与这种抑制作用的神经垂体肽受体的特异性。V1激动剂[苯丙氨酸²,鸟氨酸⁸]血管加压素([苯丙氨酸²]OVT)可抑制基础状态及胰高血糖素刺激的腺苷酸环化酶活性,并且在SW环境中的这种作用(20%)是在FW环境中(10%)的两倍。然而,V2激动剂1 - 脱氨基[缬氨酸⁴,精氨酸⁸] - 血管加压素(dVDAVP)在两种环境中产生的刺激幅度相同(10%)。V1拮抗剂[(1 - β - 巯基 - β - β - 环戊亚甲基丙酸),1 - (O - 乙基)酪氨酸²,鸟氨酸⁸]血管加压素(d(CH₂)₅[酪氨酸(乙基)²]OVT)完全逆转了AVT或IT诱导的对基础状态或胰高血糖素刺激的环化酶活性的抑制作用,而V1/V2拮抗剂[(1 - β - 巯基 - β - β - 环戊亚甲基丙酸),1 - (O - 乙基)D - 酪氨酸²,缬氨酸⁴,精氨酸⁸]血管加压素(d(CH₂)₅[D - 酪氨酸(乙基)²] - VAVP)(以前在两栖动物中用作V2拮抗剂)则没有这种作用。当具有活性时,所有类似物在10⁻¹¹ - 10⁻¹⁰ M时具有最大活性(50%最大活性约为10⁻¹³ M),这与天然肽的情况相同。这些结果与我们之前的观察结果一起,表明鳃上皮是神经垂体肽的直接靶器官,并表明鱼类中涉及的激素受体如果不是完全属于,也主要属于一种我们提议在等待进一步表征时指定为鱼类神经垂体激素(NHF)受体的新型受体。