Urinary prostaglandin and sodium metabolism in patients with essential hypertension.
Urinary prostaglandin and sodium metabolism in patients with essential hypertension.
复制标题
原发性高血压患者的尿前列腺素和钠代谢。
DOI：
10.1620/tjem.124.277
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发表时间：
1978
影响因子：
2.2
通讯作者：
K. Yoshinaga
中科院分区：
文献类型：
--
作者：
N. Yasujima;K. Abe;N. Irokawa;S. Chiba;M. Sato;M. Seino;Y. Sakurai;K. Saito;T. Ito;K. Ritsu;K. Yoshinaga
以尿前列腺素E （PGE）排泄量为指标，测定15例原发性高血压患者钠耗竭后尿醛固酮排泄量、血浆肾素活性、尿钠排泄量、尿钾排泄量，探讨肾脏PGE与钠代谢的相互作用。钠耗尽后，尿PGE排泄减少，而尿醛固酮排泄和血浆肾素活性增加。尿PGE排泄与尿钠排泄（r=0.41, p < 0.01）、尿钠排泄与尿钾排泄比（r= 0.43, p < 0.005）呈显著正相关。这些结果支持了肾脏PGE可能在钠代谢调节中发挥重要作用的假设，并且PGE的这种作用独立于肾素-醛固酮系统。
Urinary prostaglandin E (PGE) excretion as an indicator of renal PGE, urinary aldosterone excretion, plasma renin activity, urinary sodium excretion, and urinary potassium excretion were measured after sodium depletion in 15 patients with essential hypertension to investigate the interaction between renal PGE and sodium metabolism. Following sodium depletion, urinary PGE excretion decreased, whereas urinary aldosterone excretion and plasma renin activity increased. Significant positive correlations were found between urinary PGE excretion and urinary sodium excretion (r=0.41, p less than 0.01) or urinary sodium excretion-urinary potassium excretion ratio (r = 0.43, p less than 0.005). These results support the hypothesis that the renal PGE may play an important role in the regulation of sodium metabolism and this action of PGE is independent of the renin-aldosterone system.