Plasma arginine vasopressin (PAV) concentration was determined by radioimmunoassay during the diurnal cycle in 8 recombent healthy male subjects. Two subjects were studied again 3 weeks later while receiving 1 mycles. In 8 out of 10 cycles, a nocturnal increase in PAV was found; there was a progressive rise during the night in 5 subjects and a peak occurred at 2400 or 3400 h. In 1 subject no variation was detected and in another, the pattern was compleetly different. The mean PAV in the 10 cycles was significantly (P less than 0.001) higher during the night than during the day. Dexamethasone did not modify the pattern of variation, but induced a significant (P less than 0.001) decrease in PAV. Hematocrit remained stable throughout the study as did osmolality, except at 2000 h, when a significant (P less than 0.001) increase (5 mOsm) on average occurred in every subject. Blood sugar, sodium or chloride did not account for the observed rise in osmolality and no simultaneous change in PAV occurred. A rise in PAV explains, to some extent, the known nocturnal decrease in urine output. Diurnal variations in PAV must be taken into account in clinical investigations involving vasopressin.

Previous studies from this laboratory (1-4) have shown that: 1) there is a statistically significant increase in the mean urinary aldosterone excretion from groups of patients with essential, renal or malignant hypertension, as compared with that of normal subjects similarly studied; 2) 43 per cent of patients with essential hypertension have urinary aldosterone values above normal limits; 3) there is an excessive fluctuation of daily urinary aldosterone in hypertensive patients, from normal to above normal levels, which is most prominent in the early phase of the disease; and 4) mean urinary preglnanetriol is significantly decreased (p < 0.001) in the same groups of hypertensive patients, and the pregnanetriol/aldosterone ratio is below the lower limits of normal range in 92 per cent of all patients studied with arterial hypertension.The findings of a mean increase in urinary aldosterone and of its excessive daily fluctuation in hypertensive patients have recently been confirmed by Romanelli, Biancalona and Matterazzi (5), Venning, Dyrenfurth, Dossetor and Beck (6) and Schwartz (7). However, Laragh and co-workers (8), using a method devised by Ulick, Laragh and Lieberman (9) for the measurement of aldosterone secretion rate, found normal values in 8 patients with benign essential hypertension and significantly increased secretion rates in 5 of 8 pa- Hypertension, Bern, Switzerland, June 6-10, 1960. t Research Fellow of the National Research Council of Canada, 1959Canada, -1960 t Former Research Fellow of the National Research Council, Ottawa, 1957Ottawa, -1958 tients with advanced hypertension and in 14 of 15 patients with malignant hypertension. On the other hand, in a preliminary study, Muller found normal aldosterone secretion rates in patients with malignant hypertension (10).It appears however, that this disturbance in adrenocortical regulation may not be the basic or the sole factor in the pathogenesis of hypertension. Both clinical and experimental evidence strongly suggest that the kidney plays a definite role. We therefore studied the possibility of a relationship between the renal pressor system and aldosterone.Our preliminary results (11), showing a marked stimulatory effect of angiotensin II on urinary aldosteronie, have been confirmed in the present study.Seven normal subjects were studied. Continuous intravenous infusions of glucose, angiotensin, norepinephrine and phenylephrine were administered for periods of 7 to 14 hours, and urines were analyzed for sodium, potassium, aldosterone, cortisol, cortisone and their tetrahydro derivatives. The results obtained show a marked and specific tropic effect of angiotensin on aldosterone excretion. SUBJECTS AND METHODSThe subjects were 7 healthy male volunteer medical students, maintained on a fixed sodium and potassium intake (102 and 90 mEq per day, respectively) for 5 days prior to and during the experimental period. They were admitted to hospital for metabolic balance for the duration of the experiments. Urine was collected every 24 hours, except ...

Low blood pressure is frequent in the akinetic form of Parkinson's disease. A low renin activity in plasma as well as a low rate of aldosterone secretion is demonstrated in these patients. Renin activity in the plasma is further decreased by treatment with L-dihy-droxyphenylalanine, thus partially accouinting for the hypotensive episodes seen with this form of therapy.