Chen Y M, Hsieh B S, Wu K D, Chu T S
Department of Internal Medicine, National Taiwan University Hospital, Taipei, R.O.C.
J Formos Med Assoc. 1991 Oct;90(10):927-31.
Acute response in blood pressure (BP) and natriuresis to saline infusion was evaluated in 16 patients with primary aldosteronism caused by aldosteronoma (PA) and 12 patients with salt-sensitive essential hypertension (SSEH). Salt-sensitivity was defined by a decrease in mean BP exceeding 5% at the second hour after a 20 mg furosemide injection. Plasma renin activity (PRA), plasma aldosterone concentration (PAC) and urine electrolytes in response to saline infusion were determined. During a 2-liter isotonic saline infusion, a similar degree of natriuresis and change in BP were observed in PA and SSEH patients. A significantly inverse correlation between the increase in mean BP and the degree of natriuresis at the end of the infusion was found in patients with SSEH (r = -0.80, p less than 0.01). No correlation was observed between these parameters in patients with PA (r = 0.28, p greater than 0.05). These results suggest that hypernatriuresis in SSEH may play a protective mechanism against abrupt increases in BP and volume during acute saline loading. This protective mechanism was not evident in patients with PA.
对16例由醛固酮瘤引起的原发性醛固酮增多症（PA）患者和12例盐敏感性原发性高血压（SSEH）患者进行了评估，观察其血压（BP）和钠排泄对生理盐水输注的急性反应。盐敏感性定义为注射20 mg速尿后第二小时平均血压下降超过5%。测定了生理盐水输注后血浆肾素活性（PRA）、血浆醛固酮浓度（PAC）和尿电解质。在输注2升等渗盐水期间，PA患者和SSEH患者的钠排泄程度和血压变化相似。在SSEH患者中，输注结束时平均血压升高与钠排泄程度之间存在显著负相关（r = -0.80，p < 0.01）。PA患者的这些参数之间未观察到相关性（r = 0.28，p > 0.05）。这些结果表明，SSEH中的高钠排泄可能在急性盐水负荷期间对血压和血容量的突然增加起到保护机制。这种保护机制在PA患者中不明显。
