Selçuk Y, San A, Bakan E, Yiğitoğlu R
Department of Internal Medicine, Ataturk University Research Hospital, Erzurum, Turkey.
Nephrol Dial Transplant. 1991;6(8):557-61. doi: 10.1093/ndt/6.8.557.
To determine the relationship between plasma immunoreactive atrial natriuretic peptide (i-ANP) and renin-angiotensin-aldosterone system (RAAS), plasma i-ANP, plasma renin activity (PRA) and plasma aldosterone (PA) were assayed in 29 patients (19 hypertensive and 10 normotensive) with chronic renal failure (CRF), and in 10 healthy subjects. Hypertensive patients had higher i-ANP values than normotensive patients and controls (P less than 0.05 and P less than 0.01 respectively). There was no significant correlation between plasma i-ANP and creatinine concentrations in hypertensive patients, whereas this correlation was statistically significant in normotensive patients (r = 0.70, P less than 0.01). Other positive correlations were between plasma i-ANP and systolic blood pressure in hypertensive patients (r = 0.69, P less than 0.01) and between plasma ANP and mean arterial pressure in normotensive patients (r = 0.63, P less than 0.01). There was significant negative correlation between plasma ANP and fractional sodium excretion (FENa) in hypertensive patients (r = -0.47, P less than 0.05), though there was significant positive correlation in normotensive patients (r = 0.80, P less than 0.01). Hypertensive patients, with the exception of one anuric patient and another with atrial fibrillation, had a significant negative correlation between FENa and systolic arterial blood pressure (r = 0.64, P less than 0.01). The patient group had increased PRA and PA values (P less than 0.01 and P less than 0.001 respectively) and showed positive correlation with mean arterial pressure (MAP) (r = 0.71, P less than 0.001 and r = 0.58, P less than 0.01 respectively). These results show that increased concentrations of immunoreactive ANP circulate in CRF together with activated RAAS. We demonstrate that elevated ANP cannot affect blood pressure and natriuresis in hypertensive patients with CRF, whose RAAS is activated.
为了确定血浆免疫反应性心钠素（i-ANP）与肾素-血管紧张素-醛固酮系统（RAAS）之间的关系，我们检测了29例慢性肾衰竭（CRF）患者（19例高血压患者和10例血压正常患者）及10名健康受试者的血浆i-ANP、血浆肾素活性（PRA）和血浆醛固酮（PA）。高血压患者的i-ANP值高于血压正常患者和对照组（分别为P<0.05和P<0.01）。高血压患者血浆i-ANP与肌酐浓度之间无显著相关性，而在血压正常患者中这种相关性具有统计学意义（r = 0.70，P<0.01）。其他正相关关系为高血压患者血浆i-ANP与收缩压之间（r = 0.69，P<0.01）以及血压正常患者血浆心钠素与平均动脉压之间（r = 0.63，P<0.01）。高血压患者血浆心钠素与钠排泄分数（FENa）之间存在显著负相关（r = -0.47，P<0.05），而在血压正常患者中则存在显著正相关（r = 0.80，P<0.01）。除1例无尿患者和另1例房颤患者外，高血压患者的FENa与收缩动脉压之间存在显著负相关（r = 0.64，P<0.01）。患者组的PRA和PA值升高（分别为P<0.01和P<0.001），且与平均动脉压（MAP）呈正相关（分别为r = 0.71，P<0.001和r = 0.58，P<0.01）。这些结果表明，在慢性肾衰竭患者中，免疫反应性心钠素浓度升高与激活状态的RAAS同时存在。我们证明，在RAAS被激活的慢性肾衰竭高血压患者中，升高的心钠素不能影响血压和利钠作用。
