DYSREGULATION OF ATRIAL-NATRIURETIC-FACTOR IN HYPERTENSION-PRONE MAN
DYSREGULATION OF ATRIAL-NATRIURETIC-FACTOR IN HYPERTENSION-PRONE MAN
复制标题
DOI：
10.1210/jcem-71-4-944
复制
发表时间：
1990-10-01
影响因子：
5.8
通讯作者：
SHAW, S
中科院分区：
文献类型：
--
作者：
FERRARI, P;WEIDMANN, P;SHAW, S
为了评估高血压易感人群心房钠尿因子 (ANF) 缺乏的假设，我们研究了 116 名血压正常的父母 (ONorm) 或原发性高血压父母 (OHyp) 的白人后代的血浆 ANF 和其他变量。 10 名 ONorm 和 10 名 OHyp 均为年龄和身体习惯相匹配的男性，在低（70 mmol/天）和高（350 mmol/天）饮食钠摄入量 4 天后进行了研究。轻度限钠后，ONorm 和 OHyp 之间的血浆 ANF 没有差异（9.7 .+-. 0.7 与 9.0 .+-. 1.3 fmol/L）。当钠摄入量较高时，ONorm 中的血浆 ANF 增加，但 OHyp 中则没有增加（至 18.3 .+-. 1.7 vs. 11.7 .+-. 1.7 fmol/Lj/ P < 0.001）。另一方面，血浆免疫反应性 ANF (irANF) 对盐水负荷或去甲肾上腺素诱导的血压升高的急性反应在 8 ONorm 和 8 OHyp 之间没有显着差异。在自由钠摄入期间评估了另外 51 个 ONorm 和 45 个 OHyp。根据24小时尿钠排泄是否为91 mmol/m2或更低（盐摄入模式）或超过91 mmol/m2（高盐摄入）进一步细分组。在适度盐摄入量的 26 ONorm 和 21 OHyp 中（121 .+-. 6 与 116 .+-. 9 mmol）以及在高盐摄入量的 25 ONorm 和 24 OHyp 中（226 .+-. 10 与 221 .+-. 9 mmol），24 小时尿钠相似。然而，与ONorm相比，OHyp中的血浆irANF在适度钠摄入时略低（7.7 .+-. 0.7 vs. 5.3 .+-. 0.7 fmol/L；P < 0.05），在高钠摄入时显着降低（15.0 .+-. 1.3 vs. 8.0 .+-. 1.3 fmol/L；P < 0.05）。 0.001）。此外，OHyp 中血浆 irANF 与 24 小时尿钠之间关系的斜率比 ONorm 中更平坦（z 检验 = 2.4）。我们假设一种新的内分泌综合征，其特征是一些高血压易感人群在高钠摄入期间出现相对血浆 ANF 缺乏。这种功能缺陷在慢性而非急性 ANF 释放刺激期间变得明显。它是一种家族紊乱，可能会导致高血压的发生。
To evaluate the hypothesis of an atrial natriuretic factor (ANF) deficiency in hypertension-prone humans, we investigated plasma ANF and other variables in 116 white offspring of normotensive parents (ONorm) or essential hypertensive parents (OHyp). Ten ONorm and 10 OHyp, all men matched for age and body habitus, were studied after 4 days of low (70 mmol/day) and high (350 mmol/day) dietary sodium intake. After mild sodium restriction, plasma ANF did not differ between ONorm and OHyp (9.7 .+-. 0.7 vs. 9.0 .+-. 1.3 fmol/L). On high sodium intake, plasma ANF increased in ONorm, but not in OHyp (to 18.3 .+-. 1.7 vs. 11.7 .+-. 1.7 fmol/Lj/ P < 0.001). On the other hand, acute responses of plasma immunoreactive ANF (irANF) to saline loading or a norepinephrine-induced rise in blood pressure did not differ significantly between 8 ONorm and 8 OHyp. Fifty-one additional ONorm and 45 OHyp were evaluated during liberal sodium intake. Groups were further subdivided according to whether 24-h urinary sodium excretion was 91 mmol/m2 or less (modes salt intake) or more than 91 mmol/m2 (high salt intake). Twenty-four-hour urinary sodium was similar in the 26 ONorm and 21 OHyp on a modest salt intake (121 .+-. 6 vs. 116 .+-. 9 mmol) and in the 25 ONorm and the 24 OHyp on a high salt intake (226 .+-. 10 vs. 221 .+-. 9 mmol). However, compared with ONorm, plasma irANF in OHyp was slighlty lower on modest sodium intake (7.7 .+-. 0.7 vs. 5.3 .+-. 0.7 fmol/L; P < 0.05) and markedly reduced on high sodium intake (15.0 .+-. 1.3 vs. 8.0 .+-. 1.3 fmol/L; P < 0.001). Moreover, the slope of the relationship between plasma irANF and 24-h urinary sodium was flatter in OHyp than in ONorm (z test = 2.4). We postulate a new endocrine syndrome characterized by a relative plasma ANF deficiency during high sodium intake in some hypertension-prone humans. This functional defect becomes apparent during chronic, rather than acute, stimulation of ANF release. It occurs as a familial disturbance and may potentially predispose to the development of hypertension.