Nordquist Lina, Isaksson Britta, Sjöquist Mats
Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden.
Clin Exp Hypertens. 2008 Feb;30(2):151-8. doi: 10.1080/10641960801944231.
A possible natriuretic mechanism of action of oxytocin was investigated in male Sprague-Dawley rats. The effects of an intravenous bolus injection of amiloride on urine volume, potassium and sodium excretion, and osmolality were measured with and without an intravenous infusion of oxytocin in saline. Control values were obtained during the infusion of saline. Amiloride administered during an oxytocin infusion increased sodium excretion from 0.1 +/- 0.0 to 16.6 +/- 2.1 micromol/min. In animals treated with amiloride only, the sodium excretion was 4.5 +/- 0.8 micromol/min. The administration of oxytocin only resulted in a sodium excretion of 1.2 +/- 0.3 micromol/min. After the administration of oxytocin, amiloride increased urinary flow from 4.3 +/- 0.6 microl/min to 48.8 +/- 6.1 microl/min. In animals treated with amiloride only, the flow after the bolus dose was 17.7 +/- 1.8 microl/min. The administration of oxytocin only resulted in a flow of 8.5 +/- 1.6 microl/min. The amiloride-caused change in potassium excretion was not inhibited by oxytocin. In summary, the effects of amiloride were not inhibited by the actions of oxytocin. Amiloride administrated after reaching a near steady-state effect of oxytocin was found to give rise to an effect far greater than that after the administration of oxytocin or amiloride alone. It is concluded that the intrarenal natriuretic mechanisms of oxytocin do not emanate from the amiloride-sensitive sodium channels.
在雄性斯普拉格 - 道利大鼠中研究了催产素可能的利钠作用机制。在有或没有静脉输注生理盐水加催产素的情况下，测量静脉推注氨氯吡咪对尿量、钾和钠排泄以及渗透压的影响。在输注生理盐水期间获得对照值。在输注催产素期间给予氨氯吡咪可使钠排泄量从0.1±0.0微摩尔/分钟增加到16.6±2.1微摩尔/分钟。仅用氨氯吡咪治疗的动物，钠排泄量为4.5±0.8微摩尔/分钟。仅给予催产素导致钠排泄量为1.2±0.3微摩尔/分钟。给予催产素后，氨氯吡咪使尿流率从4.3±0.6微升/分钟增加到48.8±6.1微升/分钟。仅用氨氯吡咪治疗的动物，推注剂量后的尿流率为17.7±1.8微升/分钟。仅给予催产素导致尿流率为8.5±1.6微升/分钟。催产素未抑制氨氯吡咪引起的钾排泄变化。总之，催产素的作用未抑制氨氯吡咪的作用。发现在达到催产素接近稳态作用后给予氨氯吡咪产生的效应远大于单独给予催产素或氨氯吡咪后的效应。得出的结论是，催产素的肾内利钠机制并非源自氨氯吡咪敏感的钠通道。
