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In order to study the control system of plasma aldosterone in human, we examined the effects of low salt plus upright posture, angiotensin II, ACTH and potassium upon plasma renin activity, aldosterone and cortisol in five subjects who were supposed to be normal. All of the procedures, low salt diet with below 3 g of salt and 2 hr-upright posture, 0.25 mg of Cortrosyn, angiotensin infusion to increase 20mmHG of diastolic pressure for an hour, and 30 mEq of potassium infusion stimulated plasma aldosterone significantly. Furthermore, in each subject the degrees of response to each of these stimulations were almost same. In an old woman aged 68, responses to all of stimulations were significantly lower than those in other subjects. Plasma cortisol was significantly stimulated by ACTH, but slightly reduced by potassium infusion. From these results, it is certain that plasma aldosteron levels are easily affected by a small amount of changes in angiotensin, ACTH, potassium and sodium. However, responses of aldosterone to these changes seem to be decreased in old subjects.

Background Previous studies have attempted to characterize depression using electroencephalography (EEG), but results have been inconsistent. New noise reduction technology allows EEG acquisition during conversation. Methods We recorded EEG from 40 patients with depression as they engaged in conversation using a single-channel EEG device while conducting real-time noise reduction and compared them to those of 40 healthy subjects. Differences in EEG between patients and controls, as well as differences in patients’ depression severity, were examined using the ratio of the power spectrum at each frequency. In addition, the effects of medications were examined in a similar way. Results In comparing healthy controls and depression patients, significant power spectrum differences were observed at 3 Hz, 4 Hz, and 10 Hz and higher frequencies. In the patient group, differences in the power spectrum were observed between asymptomatic patients and healthy individuals, and between patients of each respective severity level and healthy individuals. In addition, significant differences were observed at multiple frequencies when comparing patients who did and did not take antidepressants, antipsychotics, and/or benzodiazepines. However, the power spectra still remained significantly different between non-medicated patients and healthy individuals. Limitations The small sample size may have caused Type II error. Patients’ demographic characteristics varied. Moreover, most patients were taking various medications, and cannot be compared to the non-medicated control group. Conclusion A study with a larger sample size should be conducted to gauge reproducibility, but the methods used in this study could be useful in clinical practice as a biomarker of depression.

The mechanism of secretion of adrenal steroid hormones from adenomas of primary aldosteronism and Cushing's syndrome was studied in 10 patients with primary aldosteronism and in 3 patients with Cushing's syndrome in in vivo and in vitro experiments. In all of the 10 patients with primary aldosteronism, ACTH stimulated aldosterone secretion from the adenomas more significantly than did angiotensin II and III. DOC and cortisol which were contained in the adenomas were also stimulated more significantly by ACTH than by angiotensin II and III. Responses of the adenomas of Cushing's syndrome to various stimulations were less than those of primary aldosteronism. Secretion of cortisol and aldosterone from the adenomas of Cushing's syndrome was stimulated by ACTH and angiotensin II to a similar degree. From these studies, it seems that secretion of adrenal steroid hormones from adenomas of primary aldosteronism is more sensitive to extradrenal stimulations than that of Cushing's syndrome, and ACTH is the main factor in the control of the secretion of adrenal steroid hormones from the adenomas.