Gross M D, Grekin R J, Gniadek T C, Villareal J Z
N Engl J Med. 1981 Jul 23;305(4):181-5. doi: 10.1056/NEJM198107233050401.
To study the role of serotonin in regulating the release of aldosterone, we gave single, oral doses of cyproheptadine, an antiserotoninergic agent, to five normal volunteers with high aldosterone levels secondary to sodium deprivation and to 14 patients with aldosteronism (six with idiopathic aldosteronism due to bilateral adrenal hyperplasia and eight with adrenal adenoma). A diet containing 150 mmol of sodium was given to the patients with spontaneous aldosteronism, and one containing 10 mmol of sodium was given to the normal subjects, for three days before treatment and throughout the study. All subjects received dexamethasone, 2 mg daily. Serum aldosterone was measured with the subject in the recumbent position before cyproheptadine administration and at 30-minute intervals for two hours afterward. Serum aldosterone fell significantly (P less than 0.025) from the basal level in the patients with idiopathic aldosteronism due to hyperplasia. No fall was observed in the normal subjects or in the patients with adenoma. No changes were seen in renin activity, cortisol, sodium, or potassium, in any group after cyproheptadine. Suppression of aldosterone with cyproheptadine suggests a serotonin-mediated aldosterone-stimulating system. Hyperactivity of this system may be the cause of idiopathic aldosteronism associated with adrenal hyperplasia.
为研究血清素在调节醛固酮释放中的作用，我们给5名因钠缺乏导致醛固酮水平升高的正常志愿者以及14名醛固酮增多症患者（6名因双侧肾上腺增生导致的特发性醛固酮增多症患者和8名肾上腺腺瘤患者）单次口服抗血清素能药物赛庚啶。对于原发性醛固酮增多症患者给予含150 mmol钠的饮食，对于正常受试者给予含10 mmol钠的饮食，在治疗前3天及整个研究期间均如此。所有受试者每天接受2 mg地塞米松。在服用赛庚啶前让受试者卧位时测量血清醛固酮，并在之后两小时每隔30分钟测量一次。因增生导致的特发性醛固酮增多症患者的血清醛固酮从基础水平显著下降（P小于0.025）。正常受试者或腺瘤患者中未观察到下降。服用赛庚啶后，任何组的肾素活性、皮质醇、钠或钾均未出现变化。赛庚啶对醛固酮的抑制提示存在血清素介导的醛固酮刺激系统。该系统的过度活跃可能是与肾上腺增生相关的特发性醛固酮增多症的病因。
