Osswald H, Gleiter C
Pharmacokologisches Institut, Universität Tübingen.
Zentralbl Chir. 1993;118(5):267-72.
Hypernatremia is caused by a water deficit. Cases with hypernatremia and dehydration appear to cluster among children and the elderly with alterations in the level of consciousness thus with no independent access to water. In general, central nervous symptoms prevail. However, thorough examination reveals impaired renal function in many such cases. Animal experiments have shown that rapid increases of the sodium concentration in the renal artery will cause a reduction of renal blood flow (RBF), glomerular filtration rate (GFR) and inhibition of renin secretion, particularly during states of sodium chloride or volume depletion (i.e. with high plasma renin activity). In any other organ hypernatremia leads to vasodilation. The kidney, however, responds with vasoconstriction which can be reversed by the adenosine antagonist theophylline. This finding led to the hypothesis that adenosine mediates the renal response to hypernatremia. Adenosine is generated by the tubules at a higher rate when the kidney is forced to reabsorb large amounts of sodium. In this concept adenosine links metabolic processes of sodium reabsorption with the regulation of organ blood flow causing vasoconstriction via adenosine receptors on the vasa afferentia. This mechanism can explain impaired renal function during acute hypernatremia. It is concluded from experimental evidence that-apart from other therapeutic measures-the recovery of impaired renal function can be improved by administration of the adenosine antagonist theophylline.
高钠血症是由水缺乏引起的。高钠血症和脱水病例似乎集中在意识水平改变因而无法自主获取水分的儿童和老年人中。一般来说,中枢神经症状较为常见。然而,全面检查发现许多此类病例存在肾功能受损。动物实验表明,肾动脉中钠浓度的快速升高会导致肾血流量(RBF)、肾小球滤过率(GFR)降低以及肾素分泌受到抑制,尤其是在氯化钠缺乏或血容量不足的状态下(即血浆肾素活性较高时)。在其他任何器官中,高钠血症都会导致血管舒张。然而,肾脏的反应却是血管收缩,而腺苷拮抗剂茶碱可以逆转这种收缩。这一发现引发了一种假说,即腺苷介导了肾脏对高钠血症的反应。当肾脏被迫重吸收大量钠时,肾小管会以更高的速率生成腺苷。按照这一概念,腺苷将钠重吸收的代谢过程与器官血流调节联系起来,通过传入小动脉上的腺苷受体导致血管收缩。这种机制可以解释急性高钠血症期间的肾功能受损情况。从实验证据可以得出结论,除了其他治疗措施外,给予腺苷拮抗剂茶碱可以改善受损肾功能的恢复。