Gómez-Alamillo C, Sanchez-Casajús A, Sierra M, Huarte E, Díez J
Division of Nephrology, San Millán Hospital, Logrono, Spain.
Kidney Int Suppl. 1996 Jun;55:S129-31.
This study was designed to investigate whether some relation exists between afferent arteriolar resistance (AAR) and the renal production of nitric oxide (NO) and prostacyclin (PGI2) in 21 patients with untreated essential hypertension and 20 normotensive controls. All subjects were studied in conditions of an unlimited Na+ diet both basally and after a four-hour amino acid infusion. AAR was calculated using Gomez's equations. Renal production of NO and PGI2 were assessed by radioimmunoassay of the urinary excretion of cGMP and 6-keto-PGF1 alpha, respectively. Baseline AAR was higher (P < 0.01) in hypertensives than in normotensives. The baseline urinary excretion of 6-keto-PGF1 alpha and cGMP were similar in the two groups of subjects. AAR diminished (P < 0.005) in normotensives and remained unchanged in hypertensives after amino acid infusion. Urinary excretion of 6-keto-PGF1 alpha was increased similarly in the two groups of subjects after infusion. Urinary excretion of cGMP remained unchanged in normotensives and decreased by 31% in hypertensives after infusion. These findings suggest that afferent vasoconstriction present in hypertensive patients is unresponsive to the vasodilatory manoeuvre of amino acid infusion. This lack of response may be due to a defective renal synthesis of NO in these patients.
本研究旨在调查21例未经治疗的原发性高血压患者和20例血压正常的对照者的入球小动脉阻力（AAR）与肾脏一氧化氮（NO）及前列环素（PGI2）生成之间是否存在某种关系。所有受试者均在基础状态及输注氨基酸4小时后，于不限钠饮食条件下进行研究。使用戈麦斯方程计算AAR。分别通过放射免疫分析法检测尿中环磷酸鸟苷（cGMP）和6-酮-前列腺素F1α（6-keto-PGF1α）的排泄量来评估肾脏NO和PGI2的生成。高血压患者的基线AAR高于血压正常者（P<0.01）。两组受试者的6-酮-前列腺素F1α和cGMP的基线尿排泄量相似。输注氨基酸后，血压正常者的AAR降低（P<0.005），而高血压患者的AAR保持不变。输注后，两组受试者的6-酮-前列腺素F1α尿排泄量均有类似增加。输注后，血压正常者的cGMP尿排泄量保持不变，而高血压患者的cGMP尿排泄量下降了31%。这些发现表明，高血压患者存在的入球小动脉收缩对氨基酸输注的血管舒张操作无反应。这种无反应可能是由于这些患者肾脏NO合成存在缺陷。
