Higgins J T, Gupta S K
Department of Medicine, Medical College of Ohio, Toledo 43699.
Prog Clin Biol Res. 1988;258:93-101.
The urinary bladder of the toad Bufo marinus has been used to examine the effect on sodium transport, measured by short-circuit current, of natural antidiuretic hormones and several synthetic peptide analogs. In mammals, these synthetic analogs show specificity for different receptors, designated V1 and V2 receptors, whose biological responses are mediated by phosphatidyl inositol breakdown products or adenylate cyclase activity, respectively. All analogs stimulated SCC, with relative potencies AVT greater than AVP greater than Phe2 OVT (V1 agonist) much greater than d(CH2)5Tyr(Me)AVP (V1 antagonist) = d(CH2)5[D-Ile2,Abu4]AVP (V2 antagonist). The V1 and V2 antagonists inhibited the SCC response to AVT and Phe2OVT, with similar inhibitory potencies. We conclude that the stimulation of sodium transport by antidiuretic hormones involves one hormone receptor which does not show the selectivity of mammalian antidiuretic hormone receptors, and may represent a more primitive type of receptor.
海蟾蜍(Bufo marinus)的膀胱已被用于研究天然抗利尿激素和几种合成肽类似物对钠转运的影响,钠转运通过短路电流来测量。在哺乳动物中,这些合成类似物对不同的受体具有特异性,分别称为V1和V2受体,其生物学反应分别由磷脂酰肌醇分解产物或腺苷酸环化酶活性介导。所有类似物均刺激短路电流,相对效力为精氨酸血管加压素(AVT)大于血管加压素(AVP)大于苯丙氨酸2 - 鸟氨酸加压素(Phe2 OVT,V1激动剂)远大于d(CH2)5酪氨酸(甲基)血管加压素(d(CH2)5Tyr(Me)AVP,V1拮抗剂)= d(CH2)5[D - 异亮氨酸2,氨基丁酸4]血管加压素(d(CH2)5[D - Ile2,Abu4]AVP,V2拮抗剂)。V1和V2拮抗剂抑制了对AVT和Phe2OVT的短路电流反应,抑制效力相似。我们得出结论,抗利尿激素对钠转运的刺激涉及一种激素受体,该受体不表现出哺乳动物抗利尿激素受体的选择性,可能代表一种更原始的受体类型。