Fadem S Z, Hernandez-Llamas G, Patak R V, Rosenblatt S G, Lifschitz M D, Stein J H
J Clin Invest. 1982 Mar;69(3):604-10. doi: 10.1172/jci110487.
The administration of vasodilating agents such as bradykinin and acetylcholine cause an increase in urinary sodium excretion. Yet the mechanisms involved in this natriuretic effect are not clear. Recent studies with another renal vasodilator, secretin have shown this drug also causes a profound increase in renal blood flow but without major changes in sodium excretion. To attempt to delineate the basis of this difference in sodium excretion with these drugs, the renal functional effects of secretin and bradykinin were compared at an equivalent vasodilating dose. Bradykinin increased renal blood flow from 222 to 342 ml/min, urine volume from 0.2 to 1.2 ml/min, and urine sodium excretion from 28 to 115 mueq/min. Urine osmolality fell from 1,230 to 401 mosmol/kg. Secretin caused a comparable increase in renal blood flow (216 to 325 ml/min) while changes in urine flow, sodium excretion, and urine osmolality were significantly less. In further studies papillary plasma flow was estimated using the albumin accumulation technique. Control papillary plasma flow was 29 ml/min per 100 g. Bradykinin increased urinary sodium excretion 108 mueq/min and decreased urinary osmolality from 1,254 to 516 mosmol/kg in association with a rise in papillary plasma flow to 62 ml/min per 100 g. Urine sodium excretion, urinary osmolality, and urine flow rate, as well as papillary plasma flow rate (32 ml/min per 100 g) were unchanged from control when secretin was administered. Studies with acetylcholine were qualitatively similar to those of bradykinin. Renal blood flow increased from 150 to 248 ml/min, urinary sodium excretion increased from 20 to 243 mueq/min, urinary osmolality decreased from 1,237 to 411 mosmol/kg and papillary plasma flow increased from 39 to 52 ml/min per 100 g. It is suggested that the natriuretic effect of some vasodilators is due, at least in part, to alterations in medullary hemodynamics, as evidenced by the increase in papillary plasma flow seen with bradykinin and acetylcholine, but not secretin.
给予缓激肽和乙酰胆碱等血管舒张剂会导致尿钠排泄增加。然而，这种利钠作用的机制尚不清楚。最近对另一种肾血管舒张剂促胰液素的研究表明，这种药物也会使肾血流量显著增加，但钠排泄没有明显变化。为了试图阐明这些药物在钠排泄方面存在差异的基础，在等效的血管舒张剂量下比较了促胰液素和缓激肽对肾功能的影响。缓激肽使肾血流量从222毫升/分钟增加到342毫升/分钟，尿量从0.2毫升/分钟增加到1.2毫升/分钟，尿钠排泄从28微当量/分钟增加到115微当量/分钟。尿渗透压从1230毫摩尔/千克降至401毫摩尔/千克。促胰液素使肾血流量有类似的增加（从216毫升/分钟增加到325毫升/分钟），而尿流量、钠排泄和尿渗透压的变化则明显较小。在进一步的研究中，使用白蛋白积聚技术估计乳头血浆流量。对照时乳头血浆流量为每100克29毫升/分钟。缓激肽使尿钠排泄增加108微当量/分钟，尿渗透压从1254毫摩尔/千克降至516毫摩尔/千克，同时乳头血浆流量增加到每100克62毫升/分钟。给予促胰液素时，尿钠排泄、尿渗透压、尿流率以及乳头血浆流速（每100克32毫升/分钟）与对照时相比没有变化。对乙酰胆碱的研究在性质上与缓激肽的研究相似。肾血流量从150毫升/分钟增加到248毫升/分钟，尿钠排泄从20微当量/分钟增加到243微当量/分钟，尿渗透压从1237毫摩尔/千克降至411毫摩尔/千克，乳头血浆流量从每100克39毫升/分钟增加到52毫升/分钟。有人提出，一些血管舒张剂的利钠作用至少部分是由于髓质血流动力学的改变，缓激肽和乙酰胆碱可使乳头血浆流量增加，而促胰液素则不然，这证明了这一点。
