STUDIES ON THE MECHANISM OF SODIUM-EXCRETION DURING DRUG-INDUCED VASODILATATION IN THE DOG
STUDIES ON THE MECHANISM OF SODIUM-EXCRETION DURING DRUG-INDUCED VASODILATATION IN THE DOG
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DOI：
10.1172/jci110487
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发表时间：
1982-01-01
影响因子：
15.9
通讯作者：
STEIN, JH
中科院分区：
文献类型：
--
作者：
FADEM, SZ;HERNANDEZLLAMAS, G;STEIN, JH
血管舒张剂如缓激肽和乙酰胆碱的给药导致尿钠排泄增加。这种利钠利尿作用的机制尚不清楚。最近对另一种肾血管扩张剂胰泌素的研究表明，这种药物也会引起肾血流量的显著增加，但对钠排泄没有重大影响。为了描述这些药物钠排泄差异的基础，在等效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 ml/min增加到342 ml/min，尿量从0.2-1.2 ml/min增加，尿Na排泄从28 μ eq/min增加到115 μ eq/min。尿渗透压从1230 mosmol/kg下降到401 mosmol/kg。促胰液素引起的肾血流量（216至325 ml/min）的增加相当，而尿流量，钠排泄和尿渗透压的变化显着less. Papillary血浆流量估计使用白蛋白积累技术。对照乳头状血浆流量为29 ml/min/100 g。缓激肽使尿钠排泄增加108 μ eq/min，并使尿渗透压从1254 mosmol/ kg降低至516 mosmol/ kg，这与乳头状血浆流量增加至62 ml/min/100 g有关。当给予促胰液素时，尿钠排泄、尿渗透压、尿流速和乳头状血浆流速（32 ml/min/100 g）与对照组相比无变化。乙酰胆碱的研究定性上与缓激肽相似。肾血流量从150 ml/min增加到248 ml/min，尿Na排泄从20 μ eq/min增加到243 μ eq/min，尿渗透压从1，237 mosmol/kg降低到411 mosmol/kg，乳头状血浆流量从39 ml/min增加到52 ml/min/100 g。某些血管扩张剂对延髓血流动力学改变的利钠作用，如缓激肽和乙酰胆碱（而非促胰液素）引起的乳头状血浆流量增加所证实。
The administration of vasodilating agents such as bradykinin and acetylcholine cause an increase in urinary Na excretion. 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 Na excretion. To delineate the basis of this difference in Na 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 0.2-1.2 ml/min and urine Na excretion from 28 to 115 .mu.eq/min. Urine osmolality fell from 1230 to 401 mosmol/kg. Secretin caused a comparable increase in renal blood flow (216 to 325 ml/min) while changes in urine flow, Na excretion and urine osmolality were significantly less. 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 .mu.eq/min and decreased urinary osmolality from 1254 to 516 mosmol/ kg in association with a rise in papillary plasma flow to 62 ml/min per 100 g. Urine Na excretion, urinary osmolality, urine flow rate and 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 150-248 ml/min, urinary Na excretion increased from 20 to 243 .mu.eq/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. The natriuretic effect of some vasodilators to alterations in medullary hemodynamics, as evidenced by the increase in papillary plasma flow seen with bradykinin and acetylcholine, but not secretin.