Ando Y, Tabei K, Asano Y
Division of Nephrology, Jichi Medical School Hospital, Tochigi, Japan.
J Clin Invest. 1991 Sep;88(3):952-9. doi: 10.1172/JCI115398.
We explored the action of luminal AVP in rabbit CCD perfused in vitro at 37 degrees C. Nanomolar concentrations of luminal AVP induced a sustained hyperpolarization of transepithelial voltage (Vt) in contrast to a transient hyperpolarization caused by basolateral AVP. 10 microM basolateral ouabain abolished the latter but not the former change in Vt. Despite a sustained hyperpolarization (from -20.7 +/- 2.9 to -34.1 +/- 4.7 mV; P less than 0.01), 10 nM luminal AVP only slightly altered net Na+ and K+ fluxes (7.6% stimulation and no significant change, respectively). Instead, luminal AVP appeared to modulate an acetazolamide-sensitive electrogenic ion transport because 200 microM basolateral acetazolamide suppressed the luminal AVP-induced hyperpolarization (percentage of Vt from -50.4 +/- 10.8 to -5.1 +/- 1.4; P less than 0.005). In terms of water transport, 10 nM luminal AVP did not change hydraulic conductivity (Lp, x 10(-7) cm/atm per s) (from 3.9 +/- 0.8 to 5.0 +/- 1.2), but suppressed the increase in Lp induced by 20 pM basolateral AVP (134.9 +/- 19.2 vs. 204.3 +/- 21.1 in control; P less than 0.05). These findings demonstrate distinct luminal action of AVP, suggesting amphilateral regulation of epithelial transport by AVP in the CCD.
我们研究了管腔血管加压素（AVP）在37℃体外灌注的兔皮质集合管（CCD）中的作用。与基底侧AVP引起的短暂超极化相反，纳摩尔浓度的管腔AVP诱导跨上皮电压（Vt）持续超极化。10微摩尔基底侧哇巴因消除了后者引起的Vt变化，但未消除前者。尽管存在持续超极化（从-20.7±2.9 mV变为-34.1±4.7 mV；P<0.01），10纳摩尔管腔AVP仅轻微改变净Na+和K+通量（分别刺激7.6%和无显著变化）。相反，管腔AVP似乎调节一种乙酰唑胺敏感的生电离子转运，因为200微摩尔基底侧乙酰唑胺抑制了管腔AVP诱导的超极化（Vt百分比从-50.4±10.8变为-5.1±1.4；P<0.005）。在水转运方面，10纳摩尔管腔AVP未改变水力传导率（Lp，×10-7 cm/atm per s）（从3.9±0.8变为5.0±1.2），但抑制了20皮摩尔基底侧AVP诱导的Lp增加（对照组为134.9±19.2 vs. 204.3±21.1；P<0.05）。这些发现证明了AVP独特的管腔作用，提示AVP对CCD上皮转运具有双侧调节作用。
