Goncharevskaya O A, Shakhmatova E I, Natochin Y V
Laboratory of Renal Physiology, Sechenov Institute of Evolutionary Physiology and Biochemistry of Russian Academy of Sciences, 44 Thorez Avenue, St. Petersburg 194223, Russia.
Pflugers Arch. 1995 Oct;430(6):1004-11. doi: 10.1007/BF01837415.
In the early distal tubule of the newt Triturus vulgaris L., 1 nM arginine-vasopressin (AVP) increased water reabsorption; the fractional reabsorption of Na+ was elevated from 46.2 +/- 6.9% to 67.8 +/- 3.9% (P < 0.001), of Cl- from 52.7 +/- 6.7% to 73.1 +/- 3.5% (P < 0.001), of Mg2+ from 48.0 +/- 7.7% to 71.7 +/- 6.3% (P < 0.001). When V1-receptors were blocked by 1 nM peptide V1-antagonist [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid), 2-(O-methyl) Tyr]-[Arg8]vasopressin, 1 nM AVP increased the fractional reabsorption of fluid by 8.9% of Na+ by 10.7% and of Cl- by 11.2%, as compared with the effect of AVP alone. The fractional reabsorption of Ca2+ after addition of AVP did not differ from control; when V1-receptors were blocked in the presence of AVP, the fractional reabsorption of Ca2+ was increased by AVP. The V1-receptor block in the presence of AVP did not change the fractional reabsorption of Mg2+. Experiments on the urinary bladder of the frog Rana temporaria L. showed that 1 nM SR 49059, a non-peptide antagonist of V1a-receptors, like the peptide V1-antagonist, enhanced the AVP effect by 29%. Inhibition of protein kinase C activity by calphostin C (1 nM) mimicked the effect of V1-antagonists; the AVP hydroosmotic effect was increased by 60%. The results obtained indicate that V1-receptors modulate the effects of V2-receptor activation: their block is accompanied by an enhancement of the AVP hydroosmotic effect in the frog urinary bladder and by an increase of Na+ and Cl- reabsorption in the newt early distal tubule. The enhancement of the AVP effect owing to the V1-receptor activation seems to be mediated by a decrease in protein kinase C activity.
在普通蝾螈（Triturus vulgaris L.）的早期远曲小管中，1纳摩尔精氨酸加压素（AVP）可增加水的重吸收；钠的分数重吸收从46.2±6.9%升高至67.8±3.9%（P<0.001），氯从52.7±6.7%升高至73.1±3.5%（P<0.001），镁从48.0±7.7%升高至71.7±6.3%（P<0.001）。当V1受体被1纳摩尔肽V1拮抗剂[1-(β-巯基-β,β-环戊亚甲基丙酸),2-(O-甲基)酪氨酸]-[精氨酸8]加压素阻断时，与单独使用AVP的效果相比，1纳摩尔AVP使液体的分数重吸收增加，钠增加了8.9%，氯增加了10.7%，氯增加了11.2%。添加AVP后钙的分数重吸收与对照无差异；当在AVP存在的情况下阻断V1受体时，AVP使钙的分数重吸收增加。在AVP存在的情况下阻断V1受体并未改变镁的分数重吸收。对林蛙（Rana temporaria L.）膀胱的实验表明，1纳摩尔V1a受体的非肽拮抗剂SR 49059与肽V1拮抗剂一样，使AVP的作用增强了29%。钙磷蛋白C（1纳摩尔）对蛋白激酶C活性的抑制模拟了V1拮抗剂的作用；AVP的水渗透作用增加了60%。所得结果表明，V1受体调节V2受体激活的作用：阻断它们会使蛙膀胱中AVP的水渗透作用增强，并使蝾螈早期远曲小管中钠和氯的重吸收增加。由于V1受体激活导致的AVP作用增强似乎是由蛋白激酶C活性降低介导的。
